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International Conference on
Immunology and Immunotechnology

November 1-3, 2017 | Barcelona, Spain

Program Schedule

  • Keynote Speaker

    Time:

    Title

    Title: Tumor suppressor WWOX: from discovery to preclinical findings

    Nan-Shan Chang
    National Cheng Kung University, Taiwan
    Biography
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    Biography

    Nan-Shan Chang
    National Cheng Kung University, Taiwan

    Dr. Nan-Shan Chang is currently the Distinguished Professor of the Molecular Medicine Institute, National Cheng Kung University (NCKU) in Taiwan, and the Adjunct Professor with the SUNY Upstate Medical University and the NYS Institute for Basic Research in Developmental Disabilities, New York. Dr. Chang is most noted for his discovery of tumor suppressor WWOX in 2000. Recent Awards: Breast cancer and neurofibromatosis research awards from the Department of Defense, USA, in 2008 and 2010; Distinguished Professor Award 2010, 2013, 2016 from NCKU; Distinguished Scientist Award 2011 from the Society of Experimental Biology & Medicine, USA.



    Abstract
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    Abstract

    Nan-Shan Chang
    National Cheng Kung University, Taiwan

    We have first discovered tumor suppressor WWOX, independently with two other groups, in 2000. Although it was originally designated as a tumor suppressor, WWOX/Wwox deficiency in the newborns of humans, mice and rats do not exhibit spontaneous tumor formation. Indeed, WWOX protein exhibits a plethora of physiological functions, including control of cancer growth and neural development and degeneration, participation of pY33-WWOX in apoptosis and bubbling cell death, integration with multiple signaling networks, and regulation of metabolism and immune cell differentiation. For example, exogenous complement C1q-mediated death of neuroblastoma and prostate cancer cells requires WWOX as an adaptor for death signaling. This type of cancer suppression is antibody-independent and a non-inflammatory action of C1q. Most recently, we have shown that during forced maturation, phorbol and calcium ionophore induce up regulation of WWOX phosphorylation at Ser14 in leukemia T cells. Furthermore, during cancer progression and neurodegeneration in vivo, target organs tend to have pS14-WWOX upregulation. Suppression of pS14-WWOX expression by Zfra (zinc finger-like protein that regulates apoptosis) results in blocking cancer growth and restoration of memory loss during neurodegeneration. The observations suggest that converting anticancer pY33-WWOX to pS14-WWOX renders enhancement of cancer growth and metastasisand progression of neuro degeneration.

    Keynote Speaker

    Time:

    Title

    Title: Profiling the IgOme - the repertoire of antibodies in polyclonal serum

    Jonathan M. Gershoni
    Tel Aviv University, Israel
    Biography
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    Biography

    Jonathan M. Gershoni
    Tel Aviv University, Israel

    Prof. Jonathan M. Gershoni completed his BSc in Biology and PhD in Biochemistry at the Hebrew University of Jerusalem. He then did Post-doctoral training with Prof. George E. Palade at Yale School of Medicine where he began his research on the interplay of viruses and their targets and the defense mechanisms of the immune system. Returning to Israel in 1983 he joined the Department of Biophysics at the Weizmann Institute of Science where he continued his study of the molecular events that govern viral infection. He subsequently joined the Laboratory of Tumor Cell Biology at the National Institutes of Health in Bethesda, MD to work with Dr. Robert C. Gallo on developing new approaches to AIDS therapy and prevention. In 1990 he returned to Israel as one of the founders of the new Department of Cell Research and Immunology at Tel Aviv University where he has served as chairman (2003-2006). Over the last decade Prof. Gershoni has focused on developing new methods for the rational design of vaccines to such pandemic diseases as AIDS, Hepatitis C, influenza and SARS. Prof. Gershoni continues to investigate the humoral response towards viral pathogens; developing computational methods to profile the IgOme-the complete repertoire of antibodies in polyclonal sera, and developing novel approaches for epitope based vaccines and next generation diagnostics.



    Abstract
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    Abstract

    Jonathan M. Gershoni
    Tel Aviv University, Israel

    Polyclonal serum consists of vast collections of antibodies. The spectrum of antibody specificities is dynamic and varies with age, physiology, and exposure to pathological insults. The complete repertoire of antibody specificities in blood, the IgOme, is therefore an extraordinarily rich source of information-a molecular record of previous encounters as well as a status report of current immune activity. The ability to profile antibody specificities of polyclonal serum at exceptionally high resolution has been an important and serious challenge which can now be met. Here we describe "Deep Panning" a methodology that merges the flexibility of combinatorial phage display peptide libraries with the power of Next Generation Sequencing to enable high resolution / high-throughput interrogation of the IgOme.

    Sessions:
    Allergology and Immunology & Immunobiology & Immunogenetics & Infection & Inflammatory Diseases & Parasitology

    Time:

    Title: Mitochondrial Hyperpolarization Induced by Complex V Restriction Maintains Naive CD8+ T cell at Check

    Michael Berger
    The Hebrew University, Israel

    Biography
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    Biography

    Michael Berger
    The Hebrew University, Israel

    Dr. Michael Berger is a Senior Lecturer at the Lautenberg Center for Immunology and Cancer Research, Institute for Medical Research Israel-Canada, The Hebrew University Medical School, The Hebrew University, Jerusalem. He completed his PhD in the Faculty of Medicine, The Hebrew University of Jerusalem, Israel. He did his Postdoc at laboratory of Prof. Bruce Beutler, Department of Genetics, The Scripps Research Institute, TSRI, CA, USA. He honored as an Excellence Teaching at Faculty of Medicine, The Hebrew University of Jerusalem, Israel.



    Abstract
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    Abstract

    Michael Berger
    The Hebrew University, Israel

    Recent thymic emigrants (RTEs) represent an immature T cell subset characterized by reduced propensity to proliferate following stimuli. Here we describe the discovery of a metabolic checkpoint modulating T cells propensity to initiate a response upon priming. We demonstrate that RTEs are phenotypically distinct from their more mature naive CD8+ T cells by reducedOXPHOS, increased glycolysis, and substantially elevated mitochondrial membrane polarization. We define mitochondrial complex V restriction as the mechanism governing these metabolic differences. Following these findings we show that mitochondrial hyperpolarization, driven by ATP synthase restriction, limits naive CD8+ T cells propensity to respond to diverse stimuli independent of ATP production. Tracing mitochondrial biogenesis in vivo, we reveal that mitochondrial polarization modulates proliferation capabilities of naive CD8+ T cells upon priming by regulating the acquisition of mitochondrial biomass. Our study defines mitochondrial hyperpolarization induced by complex V restriction as a critical checkpoint directly controlling RTEs propensity to proliferate upon stimuli allowing intact T cell population and diversity.

    Time:

    Title: Large-scale automated 3D image analysis of tissue resident leukocytes for the Infection, Immunity and Immunophenotyping Consortium

    Dmitry Ushakov
    King's College London, UK

    Biography
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    Biography

    Dmitry Ushakov
    King's College London, UK

    Dmitry S. Ushakov is a research fellow at King's College London. His research is centered on understanding the fundamental principles governing immune cell motility, maintenance and interactions, which he investigates using advanced fluorescence microscopy technologies. Recently he established a novel automated 3D image processing method enabling multiparametric analysis of cells residing in tissues. This approach was utilized for the Infection, Immunity and Immunophenotyping (3i) consortium where hundreds of mouse lines were screened revealing new genes involved in immune cell homeostasis. He now takes these findings forward to further investigate the role of the identified genes in the intraepithelial leukocyte biology.



    Abstract
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    Abstract

    Dmitry Ushakov
    King's College London, UK

    Epidermal tissue is the first line of animal defense against external factors. Mouse epidermis is populated by T cells, also known as dendritic epidermal T cells (DETC), most of which belong to V 5V 1 subset. These cells form a dense network in parallel to the network of Langerhans cells. However, it is still not clear which genes define the tissue homeostasis and functionality of these cells. As part of the Infection, Immunity and Immunophenotyping (3i) Consortium we conducted epidermal immunophenotyping of over 500 mouse gene knockouts generated by the Wellcome Trust Sanger Institute. The epidermal sheets were isolated from 16 week old C57BL/6N mice and analysed by confocal microscopy and automated 3D image quantification in order to establish the effects of gene knockouts on the number and morphology of DETC and Langerhans cells. During the course of the project over 3000 mouse samples were processed. The multiparametric analysis showed a clear sexual dimorphism in wild type mice for most data readouts. Novel phenotypes were revealed for knockout lines with an overall hit rate ~4%. As a result we identified a number of new genes which were not previously associated with immune functions opening new avenues for further in depth investigation. Particularly Hbs1l knock out mice displayed severe defects in DETC morphology. Further study usingstructured illumination microscopy showed that although Hbs1l KO DETC are still able to migrate and form the immunological synapse they do not form actin-reach protrusions which may affect function of these cells in skin stress surveillance.

    Time:

    Title: Higher Susceptibility of Allergic Rhinitis Nasal Mucosa To Influenza A Viral Infection: In Vitro and In Vivo Study

    Yung Jin Jeon
    Seoul National University, South Korea

    Biography
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    Biography

    Yung Jin Jeon
    Seoul National University, South Korea

    Research Fellow of Department of Otorhinolaryngology at Seoul National University Hospital in South Korea. She graduated from Seoul National University College of Medicine and has completed her resident training at Seoul National University Hospital. She was honored as Excellent Resident. She has done International Medical Education and Research program of University of Minnesota in 2011 and visited the Department of Otorhinolaryngology at University of Harvard Medical School as a visiting physician in 2016. She is a Ph.D. candidate in Immunology of Seoul National University and currently doing basic research focusing on respiratory allergic diseases.



    Abstract
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    Abstract

    Yung Jin Jeon
    Seoul National University, South Korea

    Rationale: We studied whether the nasal mucosa in allergic rhinitis (AR) would be more susceptible to influenza A virus (IAV) infection due to lower induction of interferon (IFN)-related immune responses. Objectives: To determine whether IFN induction would be impaired in allergic nasal mucosa and to identify which IFN was correlated with higher viral loads in IAV-infected allergic nasal mucosa. Methods: IAV mRNA, viral titers and IFN expression were compared in IAV-infected normal human nasal epithelial (NHNE, N=10) and allergic rhinitis nasal epithelial (ARNE, N=10) cells. We used in vivo model of AR (BALB/C mouse, N=10) and human nasal mucosa from healthy volunteers (N=72) and AR patients (N=29) to assess the induction of IFNs after IAV infection. Results: IAV mRNA levels and viral titers were significantly higher in ARNE compared with NHNE cells. IFN-β and -λs were induced in NHNE and ARNE cells up to 3 days after IAV infection. Interestingly, induction of IFN-λs mRNA levels and the amount of secreted proteins were considerably lower in ARNE cells. The mean IFN-λs mRNA level was also significantly lower in the nasal mucosa of AR patients. We found that recombinant IFN-λ treatment attenuated IAV mRNA levels and viral titers in IAV-infected ARNE cells and completely controlled IAV infection in an in vivo AR model. Conclusion: Higher susceptibility of the allergic nasal mucosa to IAV may depend on impairment of type Ⅲ IFN induction, and type Ⅲ IFN is a key mechanistic link between higher viral loads and control of IAV infection in allergic nasal mucosa. Keywords: Influenza A virus; type Ⅲ interferon; allergic rhinitis; nasal mucosa.

    Time:

    Title: Air Pollution Particulate Matter Exposure Up-Regulates the Expression of CD206 and TNF- alpha Production in Monocytes during in Vitro Differentiation into Macrophages

    Martha Torres
    National Institute of Respiratory Diseases, Mexico

    Biography
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    Biography

    Martha Torres
    National Institute of Respiratory Diseases, Mexico



    Abstract
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    Abstract

    Martha Torres
    National Institute of Respiratory Diseases, Mexico

    Introduction: Alveolar macrophages play a central role in the protective immune response to respiratory infections and are the first line cellular responders to inhaled particulate matter (PM) and microbial pathogens. Monocytes are recruited from blood during inflammation and then mature into alveolar macrophages. Mechanisms by which PM modulate innate responses of macrophages are not understood. Objectives: To examine the effects of PM exposure on human monocytes during in vitro differentiation into macrophages and assessphagocytosis of PM, expression of cell-surface molecules and TNF production. Methods: Peripheral blood was obtained from healthy adult volunteers (n=10). Monocytes were isolated from peripheral blood mononuclear cells by plastic adherence and positive immunomagnetic selection and exposed to PM during in vitro differentiation into macrophages for seven days. Cell morphology, proportions of cells containing PM and TNF-α production were assessed by microscopy, flow cytometry for cell-surface expression of CD14, CD16, CD33, CD36, CD163, CD206 and CD209and ELISA, respectively. Ambient PM2.5(aerodynamic diameters <2.5 um) for in vitro exposure studies, were collected with high-volume PM2.5 samplers (GMW Model 1200, VFC HVPM10, airflow rate 1.13m3/min) at the National Center for Environmental Research and Training (CENICA), Mexico City). Results: Monocytes exposed to PM during their in vitro differentiation exhibited a round morphology, while unexposed monocytes showed a non-rounded morphology and were elongated. The proportion of cells containing PM increased according to the concentration of PM with the highest proportion of cells containing PM being 22% (15-32, 10g/mL). Exposure to 1, 5 and 10g /ml of PM did not show significant changes to the cell-surface expression of CD14, CD16, CD163 and CD33. Although exposure to 1, 5 and 10g/ml of PM did not significantly alter the expression of CD36 a trend to a decrease in proportion of cells expressing CD36 was observed when PM concentrations were increased. The expression of CD206 was significantly increased in cells exposed to 10g /mL of PM (p<0.005). In addition, exposure to 10g /mL of PM induced significant production of TNF- in comparison to non-exposed cells (p<0.005). Conclusions: In vitro exposure to PM enhanced the expression of CD206 and production of TNF during macrophage differentiation. Our data support the hypothesis that PM affects the differentiation of monocytes to macrophages and modify macrophage function.

    Time:

    Title: The Effects of Silver Nanoparticles on RAW 264.7 Macrophages and Human Whole Blood Cell Cultures

    Kim Lategan
    University of Western Cape, South Africa

    Biography
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    Biography

    Kim Lategan
    University of Western Cape, South Africa

    Currently concluding her PhD research project in the Medical Bioscience Department at the University of the Western Cape. She is also currently the lab manager for our Ecotoxicology/ Immunotoxicology Laboratory. Her work includes investigating the in vitro effects of heavy metals and nanoparticles on the immune system. She has previously presented work at various international conferences. These include the 16th International Symposium on Toxicity Assessment (ISTA), 7th Society of Environmental Toxicology and Chemistry (SETAC) Africa conference and the ChinaAfrica Water Forum.



    Abstract
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    Abstract

    Kim Lategan
    University of Western Cape, South Africa

    Silver nanoparticles (AgNPs) are commonly found in consumer products due to their antimicrobial properties. However, very little is known about the effects of AgNPs on the immune system. This study evaluates the effects of AgNPs on the murine macrophage cell line RAW 264.7 and human whole blood cell cultures (WBCs). The effects of AgNPs were assessed in the presence or absence of a mitogen, lipopolysaccharide (LPS). The effects of AgNPs on WBCs were monitored under basal conditions, LPS or phytohaemmagglutinin (PHA). A number of parameters were evaluated for both cultures, which included cytotoxity, biomarkers of inflammation, cytokines of the acquired immune system and a proteome profile analysis. AgNP concentrations tested had no effect on RAW cell viability. However, cytotoxicity of WBCs was evident at 250 μg/ml AgNP. Under basal conditions, AgNPs concentrations ≥ 62.5 μg/ml and > 25 μg/ml induced inflammation in RAW cells and WBCs respectively. Under a simulated inflammatory response (+ LPS), 250 μg/ml AgNP inhibited the inflammatory response for both RAW and WBCs. The acquired immune cytokines IL-10 and IFNγ were both induced by 250 μg/ml AgNP in the absence of PHA. While IL-10 was partially inhibited by 250 μg/ml AgNP in a simulated (+ PHA) acquired immune response. Proteome profiles of RAW cell supernatants show that AgNPs do in fact modulate specific protein synthesis. Upregulated RAW cell proteins due to AgNP exposure indicate induction of proteins associated with inflammation and wound and tissue healing. The mitogen activated WBCs proteome analysis indicates the partial inhibition of inflammatory proteins. Monitoring those proteins in future experiments will give a better indication of the effects of AgNPs.

    Time:

    Title: Pseudomonas aeruginosa bacteria activates chloride ion channels in immune cells

    Hani M. Alothaid
    University of Sheffield, UK

    Biography
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    Biography

    Hani M. Alothaid
    University of Sheffield, UK

    Hani M. Alothaid is a first-year PhD student at the University of Sheffield in the UK. Hani interests in the field of immunopathophysiology. His research focuses on regulation of calcineurin (Cn) as a switch in cell secretion. The regulation of cellular processes by cAMP/PKA-dependent Cn is currently not well understood. He will investigate PKA-dependent Cn regulation of chloride ion secretion in epithelia, such as seen in Cystic Fibrosis, and the release of pro-inflammatory molecules in human monocytes, such as cytokines. His research is likely to identify targets or markers that could be exploited for treatment strategies and clinical usages.



    Abstract
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    Abstract

    Hani M. Alothaid
    University of Sheffield, UK

    Cystic fibrosis (CF) is a disease that affects respiratory function and in the UK it affects about 151 young persons per 100,000 people. The disease arises due to dysfunction in cystic fibrosis transmembrane conductance regulator (CFTR) protein, a protein that has been shown recently to influence calcineurin activities in cell secretion. CFTR dysfunction causing mucus lodging and bacteria colonisation of the airways and intestinal linings leading to functional alterations of immune cells. In airways, CFTR has been shown to form a functional complex with S100A10 and AnxA2 in a cyclic adenosine monophosphate (cAMP)/ protein kinase A (PKA) dependent pathway. The multiprotein complex of CFTR, S100A10 and AnxA2 is also regulated by protein phosphatase 2B (PP2B). The objective of this study was to investigate whether chloride ion (Cl−) channels are activated by lipopolysaccharide (LPS) from Pseudomonas aeruginosa (PA), and whether this activation requires cAMP/PKA/PP2B pathway. Human monocytes and macrophages were used in the study. Whole cell patch records showed that LPS from PA can activate Cl− channels, and this activation appears to require an intact PKA/PP2B signalling pathway. The Gout in the presence of LPS was 2185.97+/-226 μS/cm2 (n=27). Gout was significantly inhibited by diisothiocyanatostilbene-disulfonic acid (DIDS), an outwardly-rectifying Cl−channel (ORCC) blocker, 1204.40+/-132 μS/cm2 in the presence of DIDS. CFTR channels were inhibited using CFTRinh172 and this reduced Gout to 838.68+/-101 μS/cm2. Data from cells stimulated with LPS from PA that were pre-incubated with PKA inhibitor or PP2B inhibitor showed no DIDS and CFTRinh172 sensitive currents. Activation of both CFTR and ORCC is therefore observed in response to exposure of monocytes and macrophages to LPS. Ongoing work is investigating whether this activation plays a subsequent role in the release of pro-inflammatory molecules.

    Time:

    Title: Parasite-Host Interaction in the Plasmodium Vivax Malaria from Brazilian Amazon Region: Immunological Clues and the Parasite Density

    Ricardo Luiz Dantas Machado
    Federal Fluminense University, Brazil

    Biography
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    Biography

    Ricardo Luiz Dantas Machado
    Federal Fluminense University, Brazil

    Ricardo Luiz DantasMachado, Ph. D. is a Full Researcher at Malaria Immunogenetics Laboratory of the Evandro Chagas Institute, Brazilian Ministry of Health. He received his degree in Pharmacisty from Universidade Federal Fluminense, Niteroi, Brazil in 1984 and his Ph.D. in Parasitology from Universidade Federal do Para, Belem, Brazil in 2001. He is an Associate Editor of the BMC Infectious Diseases, and serves on the editorial board of ISRN-AIDS and World Journal of Clinical Infectious Diseases. His main fields of research are coccidian diagnosis, molecular epidemiology and host-parasite relationship. He has published several scientific peer-reviewed papers, reviews and book chapters.



    Abstract
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    Abstract

    Ricardo Luiz Dantas Machado
    Federal Fluminense University, Brazil

    Background: P. vivax is the most prevalent species in the Brazilian Amazon region. A growing body evidences indicates that the immunity is important in the outcome of P. vivax infection. Single-nucleotide polymorphisms (SNPs) in cytokine genes can alter the production of these proteins and consequently affect the parasite density, which has been recognized as an important factor in the outcome of malaria infection. Materials and Methods: We investigated whether SNPs in cytokine genes are associated with parasite density in 50 malaria patients and 79 healthy individuals from Itaituba, municipality situated on southwest of Pará state. Three SNPs, TNFA -308G/A (rs1800629), INFB +874T/A (rs2430561), IL6 -174G/C (rs1800795) and the haplotype IL10 -1082G/A (rs1800896), -819C/T (rs1800871) and -592C/A (rs1800872), were analyzed by PCR-SSP. The parasite density was determined by counting the number of parasite in 100 separate fields and converted to the number of parasites per microliter of blood assuming 8,000 leucocytes/ µL. The existence of association was determined by Mann-Whitney test, with level of significance of 0.05, using Graph-Pad Prism software, version 6.0. Results: Parasite density levels ranged from 30 to 60,000 parasites/ mm3 (10910.4 ± 14406.25) and all SNPs tested were in Hardy-Weinberg equilibrium. No significant association was found between the SNPs tested and parasite density. Conclusions: Due to the obvious importance of cytokine effects on malaria, studies that elucidate the complex host-parasite interaction may be useful for understood pathophysiology. In the present study, the SNPs in cytokine gene appear to have no effect on the parasite density, since no association was found. The inclusion of a larger number of samples may confirm this assertion and therefore may have been a limitation of the study. Keywords: Polymorphisms, Cytokine, Parasite Density, P. vivax.

    Time:

    Title: IFN-α Boosting of Mycobacterium Bovis Bacillus Calmette Guerin (BCG)-Vaccine Promoted Th1 Type Cellular Response and Protect against M. Tuberculosis Infection

    Gloria G Guerrero M
    Autonomous University of Zacatecas, Mexico

    Biography
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    Biography

    Gloria G Guerrero M
    Autonomous University of Zacatecas, Mexico

    Dr Guerrero obtained his PhD from the National Autonomous University of Mexico. Thereafter, he did two post doctorates. One of them in the Institute of Biology of Institute Pasteur in Lille, France under the supervision of Dr Camille Locht. The second postdoc was in the lab of Jean Laureant Casanova, working with the human tuberculosis. Right after that hespent almost two years in the Institute Superiore di Sanita in Rome, Italy in which he started to work with interferon alpha and the role in mycobacterial infections. He is the head of the Molecular Biochemistry and Immunobiology lab in the Unit of Biological Science of the University Autonomous of Zacatecas in Zacatecas State Mexico. His principle interest in the study of the molecular mechanism of tuberculosis in the three models, bovine, human and using the murine model, with the aim to identify biomarkers that can be used potentially in therapy and candidate vaccines.



    Abstract
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    Abstract

    Gloria G Guerrero M
    Autonomous University of Zacatecas, Mexico

    Th1 type cellular activity plays a key role for the control of M. tuberculosis (MTb) as well as the induction of long-term memory conferring protective immunity. In order to better understand Mtb-specific immune mechanisms, both cellular and innate immune responses should be taken into account and the role of pivotal cytokines orchestrating their complex interactions should be elucidated. Type I interferons (IFN-I)(α/β) are an important family of infection-induced cytokines that among other multiples functions, promote differentiation/activation of DCs in both human, and participate in the regulation of the Th1 responses. However, contrasting and controversial results have been provided against microbial infections either in vivo as well as in vitro. At this point, our group have reported that IFN-alpha associated to BCG protects against M. lepraemurium, a mice pathogen elicited a similar skin lesion than M. leprae in adults persons with a concomitant increase in NO synthase. In the present work, we are reporting that under a specific experimental protocol of prime-boost settings, IFN-alpha boosting of BCG vaccine in mice and/or in human cell lines (A549, macrophages derived from PBMC), elicited IFN-γ, TNF-α, as well as IL-17, correlated with the induced protection against M. tuberculosis. Altogether, the data strengthened IFN-alpha as a potential candidate boosting of BCG immunity.

    Time:

    Title: Genetics, Genomics and Epigenomics approaches to identify key players in SLE

    Shaheen Khan
    UT Southwestern Medical Center, USA

    Biography
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    Biography

    Shaheen Khan
    UT Southwestern Medical Center, USA

    Shaheen Khan is an Instructor in Department of Immunology at UT Southwestern Medical Center. She received her Ph.D in Genetics from Texas A & M University where she studied molecular mechanisms underlying estrogen-mediated breast cancer. She then did her post-doctoral training at UT Southwestern Medical Center in Department of Immunology. During this time she received extensive training in the field of immunology, mouse genetics and next generation sequencing technologies. She utilizes these approaches to address key questions of her own research interests. Her current research focuses on understanding genetic Basis of autoimmunity in mice as well as SLE/Pediatric lupus patient cohorts. She also has a deep interest in translational studies in the field of cancer immunotherapy and collaborates with clinicians at Simmons Cancer Center at UT Southwestern Medical center. This study is specifically focused to understand roles of patient's genetic and immune status in development of toxicity in patients undergoing immune checkpoint blockade therapy.



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    Abstract

    Shaheen Khan
    UT Southwestern Medical Center, USA

    Systemic lupus erythematosus (SLE) is a complex chronic multisystem autoimmune disease with extensive clinical heterogeneity. Identification of novel genes in SLE has been challenging in the field due to complex genetics and epigenetics underlying disease pathogenesis. One of my research interests focuses on understanding genetic basis of SLE and identifying novel genes using state of the art next generation sequencing technologies. I have extensively used NZM2410 spontaneous mouse models of SLE to identify novel candidate genes using congenic dissection strategy combined with genomics and epigenomics approaches. My talk will focus on identification of KLF13 as a novel transcription factor that drives SLE pathogenesis by modifying the chromatin landscape of immune cells. In support of plethora of emerging studies, this study sheds light on the importance of non coding variations associated with epigenetics marks as regulators of inflammation and autoimmunity. I will also present our recent work and discuss new candidate genes that we have identified in SLE.

  • Sessions:
    Reproductive Immunology & Transplantation Immunology & Tumor and Cancer immunology & Veterinary Immunology and Immunopathology & Virology

    Time:

    Title: Transcriptomic and Epigenetic Analysis in Human Neonate T Cells

    Maria Angelica Santana
    Autonomous University State of Morelos, Mexico

    Biography
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    Biography

    Maria Angelica Santana
    Autonomous University State of Morelos, Mexico

    Dr. Santana studied her BSc. at the Universidad Autonoma Metropolitana in Mexico City. She obtained her PhD degree from Universite Louis Pasteur in Strasbourg, France and did posdoctorate work at the Medical School of The University of Manchester and at the Institute of Biotechnology, Universidad National Autonoma de Mexico. She now directs the Laboratory of Cellular Immunology at the Centro de Investigacion en Dinamica Celular, Universidad Autonoma del Estado de Morelos in Mexico. She has over 30 publications and has been responsible for national and international projects.



    Abstract
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    Abstract

    Maria Angelica Santana
    Autonomous University State of Morelos, Mexico

    Human neonates have a poor response to intracellular pathogens, despite a high inflammatory response. This leads to a high morbidity and mortality rates, reaching 37% of deaths of children under 5 years of age. A major cause of death is infections and inflammatory syndromes, like sepsis. To better understand this phenomenon, we evaluated the transcriptome and epigenomic landscape of naive CD8+- and CD4+- T cells from neonate and adult blood. Weshow that neonatal T cells have a specific genetic program established by epigenetic mechanisms, biased towards innate immunity.Functional studies corroborated that CD8+ T cells are less cytotoxic and transcribe antimicrobial peptides. CD4+ T cells have a high expression of negative TCR signalling molecules and a low expression of positive signalling molecules, explaining the high threshold of activation of these cells. Altogether, these properties could explain the high susceptibility of neonates to infections and inflammation and will contribute to a better diagnosis and management of the neonatal immune response.

    Time:

    Title: Ser14-phosphorylated WWOX induces T, B and NK cell expansion whereas dephosphorylated WWOX activates Z cell to suppress cancer growth

    NanShan Chang
    National Cheng Kung University, Taiwan

    Biography
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    Biography

    NanShan Chang
    National Cheng Kung University, Taiwan

    Dr. Nan-Shan Chang is currently the Distinguished Professor of the Molecular Medicine Institute, National Cheng Kung University (NCKU) in Taiwan, and the Adjunct Professor with the SUNY Upstate Medical University and the NYS Institute for Basic Research in Developmental Disabilities, New York. He is most noted for his discovery of tumor suppressor WWOX in 2000. Recent Awards: Breast cancer and neurofibromatosis research awards from the Department of Defense, USA, in 2008 and 2010; Distinguished Professor Award 2010, 2013, 2016 from NCKU; Distinguished Scientist Award 2011 from the Society of Experimental Biology & Medicine, USA.



    Abstract
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    Abstract

    NanShan Chang
    National Cheng Kung University, Taiwan

    Forced maturation of leukemia T cells requires upregulation of Ser14 phosphorylation of WWOX and the WWOX/ERK/IκBα signaling. WWOX is generally regarded as a tumor suppressor. Here, we showed that synthetic pSer14-WWOX7-21 peptide significantly induced the expansion of CD3+, CD4+, CD8+, and CD8+ T and CD19+ B cells in the spleens of immune-competent BALB/c mice bearing with melanoma. Despite immune cell expansion, no cancer growth suppression was observed. Notably, restoration of immune cells occurred in naiveimmunodeficient NOD-SCID mice during prolonged treatment with pSer14-WWOX7-21. In stark contrast, non-phosphorylated WWOX7-21 and WWOX7-11 peptides caused spleen Hyal-2+ CD3- CD19- or Z cells to undergo clonal expansion for blocking melanoma growth and metastasis and breast cancer growth. Both peptides induced the expression of spleen Z cells with upregulation of Hyal-2, Zfra, Noxa, Fam46A and Ademdec1 expression. Stimulation of mice with Hyal-2 antibody or sonicatedhyaluronan (HAson) activated Z cells to suppress cancer growth in vivo. In contrast, native hyaluronan (HAn) had no inhibitory effect. Time-lapse microscopy showed that activated Z cells aggressively bound and caused explosion of breast 4T1 cancer cellsin vitro. In addition, WWOX7-21 enhanced ceritinib or U0126/protease inhibitor cocktail-induced 4T1 stem cell sphere explosion, whereas pSer14-WWOX7-21 protected the cells from death. Together, our observations suggest that pSer14-WWOX supports T and B cell expansion, whereas de-phosphorylated WWOX blocks cancer growth via induction of Z cells or direct assistance of therapeutic chemicals. Ser14 phosphorylation probably switches WWOX from a tumor suppressor to promoter.

    Time:

    Title: Effects Of Group-Housed Gestating Sow Nutrition, Environment And Social Rank On Piglet Immune Responsiveness To Weaning

    Janeen Salak-Johnson
    University of Illinois, USA

    Biography
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    Biography

    Janeen Salak-Johnson
    University of Illinois, USA

    Dr. Janeen Salak-Johnson obtained her BS, MS, and PhD degrees in Animal Science from Texas Tech University. After earning her PhD in 1994, she was awarded a NIH Postdoctoral Training Fellowship in Psychoneuroimmunology and a NIH-NSRA Pain Fellowship in Pain at the University of Minnesota. She specialized in the areas of immunology, virology, and pain. In late 1999, she joined the faculty at the University of Illinois in Animal Sciences. She has authored or co-authored over 150 refereed publications, proceedings, and abstracts and given over 80 presentations in areas of Stress Physiology and Animal Well-being and Animal Behaviour and Care.



    Abstract
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    Abstract

    Janeen Salak-Johnson
    University of Illinois, USA

    The consequences of prenatal stress exposure of gestating sows on the immune responsiveness of her progeny is not well understood. The objective was to assess the effects of social rank, and diet and feeding stall treatments of gestating sows on immune status of her progeny. Pigs (n =40) born to dominant (DOM) and submissive (SUB) sows that were housed in group-pens with different feeding stalls [0.6 m (SHT) or 1.8 m (LNG)]and fed modified gestation diets [wheat middlings andsoybean hulls (MID-SOY) or distillers dried grains and corn germ-meal (DDG-GM)] were used in this study. Blood samples were collected. Total IgM was less (P = 0.01) in pigs from SUB fed DDG-GM, but cortisol was greater (P = 0.05) in pigs from SUB fed MID-SOY (social*diet). Total IgG (P < 0. 01) and IgG1:IgG2 (P < 0.01) were greater in pigsfrom sows in LNG and fed DDG-GM, but ConA(P = 0.05) and IgM (P = 0.02) were greater in pigs from sows fed MID-SOY (diet*stall).LPS-induced (P <0.01) and cortisol (P < 0.01) were greater in pigs from sows fed DDG-GM. Total IgG (P < 0.01) and IgM (P <0.01) were greater in pigs from sows in pens with LNG. Pigs from SUB had higher IgG2 (P <0.01), but pigs from DOM had higher (P = 0.10)IgG1:IgG2. These data imply that sow social rank and dietary treatment and environment during gestation may affect the immune responsiveness of her progeny.

    Time:

    Title: Modulating the Metabolic Checkpoint to Improve Cancer Immunity

    Pearlie Epling-Burnette
    Moffitt Cancer Center & Research Institute, USA

    Biography
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    Biography

    Pearlie Epling-Burnette
    Moffitt Cancer Center & Research Institute, USA

    P.K. Epling-Burnette, PharmD, PhD is a researcher at the H. Lee Moffitt Cancer Center & Research Institute and a Professor at the University of South Florida (USF) in Tampa, Florida, USA. Her laboratory program focuses on novel therapies that overcome basic mechanisms of T lymphocyte and NK cell immune suppression. Dr.Epling-Burnette has an established track record of research in hematological malignancies including myelodysplastic syndromes (MDS) which has contributed to the discovery of cereblon and its role in metabolite regulation in T cells. Her research has identified several mechanisms that contribute fundamentally to cancer-associated immune suppression through translational studies.



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    Abstract

    Pearlie Epling-Burnette
    Moffitt Cancer Center & Research Institute, USA

    Checkpoint blocking antibodies have dramatically changed the landscape of therapy in melanoma and are rapidly improving the outcome of many cancer patients. There is still an unmet clinical need to develop novel therapeutic combinations that target mechanism of tumor immune suppression toenhance the duration of response or the number of respondersafter checkpoint blockade. We found that cereblon (Crbn), an E3-ubiquitin ligase substrate receptor for the DDB1/Cul4A/Roc1 complex, genetic deficiency markedly improves effector T-cell function in the B16 melanoma mouse model. T-cells present in this hostile tumor microenvironment are exposed to hypoxia, high lactic acid, and poor nutrient availabilitythat limit their anti-tumor cytotoxic potential. While similar total intratumoral T-cells and splenic populations are presentin tumor-bearing Crbn-/-mice, the proportion of CD44+ melanoma reactive (TRP2+) tumor infiltrating lymphocytes (TIL) was increased significantly relative to Crbn+/+ mice. To explore this mechanistically, differentially-regulated genes and metabolic profiling demonstrated an increase in the uptake and metabolism of intermediates in the Arginine/Proline pathway. This pathway was also modulated by immunomodulatory drugs pomalidomide and CC-122 by suppressing CRBN function. Therefore, treatment with immunomodulatory compounds that block CRBN may act to overcome a metabolic checkpoint induced through nutrient restrictions in the tumor microenvironment.

    Time:

    Title: InvitroHIV-1 reverse transcriptase inhibition by alkaloids isolated from leaves of Ecliptaalba

    Estari Mamidala
    Kakatiya University, India

    Biography
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    Biography

    Estari Mamidala
    Kakatiya University, India

    Dr. Estari Mamidala, completed his B.Sc in Kakatiya University and did post graduation in Zoology in Department of Zoology, Kakatiya University, Telangana State India. He did his Ph.D in the same University on 'HIV prevalence in rural areas and understanding of its pathogenesis'. He attended 32 national and international conferences and presented papers and he published 28 research publications in reputed journals and doing his post-doctoral research. He received Rapid Grant Young Investigator Award and also received DST-Young Scientist project from DST, India at the time his post doctoral research. He did vaccine trial on SIV at Department of Microbiology, Emory University, Atlanta, USA during his post-doctoral research.



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    Abstract

    Estari Mamidala
    Kakatiya University, India

    Background: The current treatment modality for HIV/AIDS is HAART (Highly active anti-retroviral therapy) but this treatment is not an ultimate cure to HIV/AIDS. Therefore there is need to develop inexpensive alternativeanti-HIV/AIDS therapy. Different parts of Ecliptaalba crude extracts are used traditionally for the treatment of several diseases of liver, skin, stomach and Sexually transmitted infections. Objective: The objective of this study is to isolate alkaloid from E. alba leaves for their activities against HIV-1 reverse transcriptase. Methods: Collected leaves of E. alba were extracted with different solvents and the purity of isolated alkaloids was checked by TLC and qualitative phytochemical analysis and total alkaloids were quantified.Peripheral Blood Mononuclear Cells (PBMCs) isolated from healthy donors by ficoll-hypaque density gradient centrifugation method. Cell viability test was performed on all crude extracts by MTT assay against PBMC and HIV-1 RT inhibition activity was determined by HIV-1 Reverse Transcriptase (p66) Capture ELISA. Results: In the HIV-1 reverse transcriptase assay, the isolated alkaloid showed 89% of HIV-1 reverse transcription with IC50 of 5 ug/ml. MTT assay revealed that, the alkaloid isolated from E. alba had no cytotoxic activity (IC50 values higher than 100 ug/ml). Characterization of important biologically-active alkaloid from E. albaplant will certainly be helpful in protecting and treating various viral diseases in human beings. Conclusion: The results of the present study support the medicinal usage of the alkaloid isolated from the leaves of E. alba can be used as antiviral agents and can be subjected to characterize the therapeutic drugs and undergo further pharmacological screening that can be used as sources for new drugs. Keywords:Ecliptaalba, alkaloid, HIV-1 reverse transcriptase, MTT assay, PBMCs.

    Time:

    Title: Production of the Human single chain-transbodies against NS5A leading to Hepatitis C virus replication inhibition

    KittiratGlab-ampai
    Mahidol University, Thailand

    Biography
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    Biography

    KittiratGlab-ampai
    Mahidol University, Thailand

    KittiratGlab-ampai is a last-year Ph.D. student in Immunology program, Faculty of Medicine Siriraj Hospital, Mahidol University, Thailand. His research focuses on the production of antibodies to infectious diseases, especially Hepatitis C. He received the Royal Golden Jubilee Ph.D. scholarship, Thailand research found. Kittirat interests in the field of immunology and virology. His Ph.D. work was published in Biochemical and Biophysical Research Communications Journal, 2016. He also briefly had a research over Zika virus while working in Australia which is a part of the recent publication in Scientific Reports journal, 2017.



    Abstract
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    Abstract

    KittiratGlab-ampai
    Mahidol University, Thailand

    Hepatitis C virus (HCV) infects ~3% of world population causing chronic hepatitis which frequently leads to liver fibrosis, cirrhosis, and hepatocellular carcinoma. NS5A is a multifunctional and pivotal protein which has an important role in the viral replication, the virus morphogenesis, and pathogenesis. Thus, the NS5A protein is an attractive novel anti-HCV target In this study, human single chain (HuscFv) that inhibited the bioactivity of HCV was generated using antibody phage display library as the antibody producing tools for the ultimate purpose of developing further as a safe, side effect free and viral mutation tolerable novel anti-HCV remedy. Recombinant (r) NS5A was produced, purified, and used as bait for fishing out phage clones that displayed the NS5A-HuscFv from the established HuscFv phage display library. Based on indirect ELISA and Western blot analysis, 5 phage transfected E. coli clones produced rNS5A-bound-HuscFvs. The HuscFvs of these E. coli clones were linked to a cell penetrating peptide (Nonaarginine; R9) to make cell penetrating format. The R9-HuscFvs did not cause cytotoxicity, entered the huh7 cells (transbodies) and inhibited HCV replication (significantly reduced HCV RNA). The HCV-infected cells treated with the transbodies had up-regulation of the innate immune response genes. Computerized homology modeling and intermolecular docking (simulation) indicated that the HuscFvs formed interface contact with several critical residues of NS5A leading to interference with the protein functions and hence HCV replication inhibition. The transbodies produced in this study are worthwhile developing and testing further for future use as safe, interferon-free, broadly effective and robust DAAs.

    Time:

    Title: Targeted inhibition of Interleukin-10 accelerates microvascular rejection in mouse model of orthotopic airway transplantation

    Mohammad Afzal Khan
    Comparative Medicine Department and Organ Transplant Centre, Saudi Arabia

    Biography
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    Biography

    Mohammad Afzal Khan
    Comparative Medicine Department and Organ Transplant Centre, Saudi Arabia

    Mohammad Afzal Khan earned his PhD in Biotechnology from Aligarh Muslim University, India, and spent eight years as a post-doctoral fellow at Stanford University, USA. His primary research interests are in the field of lung transplant rejection, cell and complement-based Immunotherapies.



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    Abstract

    Mohammad Afzal Khan
    Comparative Medicine Department and Organ Transplant Centre, Saudi Arabia

    Introduction: Microvascular injuries due to excessive inflammatory responses has been associated with transplant malfunctions, which play a major role in the development of chronic rejection in all solid organ transplants, and as reported in both clinical and preclinical studies that there are no ongoing immunosuppressive regimens sufficiently affect the restoration of functional microvascular flow during the transplantation. Microvascular reestablishment, and repair during rejection is a promising new avenue to prevent acute and chronic rejection with Tregulatory cell (Treg) mediated immunosuppression but the direct molecular correlations between Treg and microvascular reestablishment has never been examined before. The present study was designed to analyze the molecular mechanisms of Treg-mediated restoration of microvascular flow during the state of immunotolerance and, in particular, the allograft rejection microenvironment. Methods: We depleted IL-10 in BALB/cJC57Bl/6J allografts, and serially monitored peripheral and graft infiltrating Tregs, key proinflammatory and regulatory cytokines, donor-recipient microvascular connections, microvascular leakiness, tissue oxygenation and microvascular blood flow during four week in orthotopic mouse airway transplants. Results: We demonstrated that depletion of IL-10 in BALB/cJC57Bl/6J allografts significantly suppressed CD4+CD25+FOXP3+ Tregs and regulatory IL-10 while upregulated major proinflammatory cytokines,IL-1β, IFN-γ and IL-15, and thereby facilitateddonor-recipient microvascular associated injuries followed by a steep drop in tissue oxygenation, microvascular blood flow levels, which proceeds subepithelial injuries at d8, d10 and d28 post transplantation. Conclusion: Altogether, these findings demonstrate that the targeted blocking of IL-10 severely affected the establishment of microvascular connections between donor-recipients graft, which are regulated through IL-10 and T regulatory cells.

    Sessions:
    Poster Session

    Time:

    Title: Allosteric induction of the CD4-bound conformation of HIV-1 gp120

    Anna Roitburd-Berman and Chen Piller
    Tel Aviv University, Israel

    Biography
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    Biography

    Anna Roitburd-Berman and Chen Piller
    Tel Aviv University, Israel

    1) Anna Roitburd-Berman completed her B.Sc. in Biology at the George S. Wise Faculty of Life Sciences, Tel Aviv University in 2005 and proceeded with her studies in the Direct Ph.D. Program at the Department of Cell Research and Immunology, Tel Aviv University. Over the past 10 years she has been studying the interaction between the HIV-1 envelope glycoprotein, gp120, and its cellular receptor, CD4, in an attempt to harness this interaction and the resulting conformational change in gp120 for the construction of a novel immunogen for HIV-1. 2) Chen Piller completed her B.Sc. in Biology at the Department of Life Sciences, Ben-Gurion University of the Negevin 2012 and proceeded to complete her M.Sc. studies at the Department of Zoology, Tel Aviv University, in 2015. Since starting her Ph.D. in 2016, at the Department of Cell Research and Immunology, Tel Aviv University, she is focusing in generation of novel Epitope-based vaccine candidates, developed to specifically focus the immune response towards neutralizing viral epitopes.



    Abstract
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    Abstract

    Anna Roitburd-Berman and Chen Piller
    Tel Aviv University, Israel

    Background: HIV-1 infection of target cells is mediated via the binding of the viral envelope protein, gp120, to the cell surface receptor CD4. This interaction leads to conformational rearrangements in gp120 forming or revealing CD4 induced (CD4i) epitopes which are critical for the subsequent recognition of the co-receptor required for viral entry. The CD4-bound state of gp120 has been considered as a potential immunogen for HIV-1 vaccine development. In this research we propose an alternative means to induce gp120 into the CD4i conformation. Results: Combinatorial phage display peptide libraries were screened against HIV-1 gp120 and short (14aa) peptides were selected that bind the viral envelope and allosterically induce the CD4i conformation . The lead peptide was subsequently systematically optimized for higher affinity as well as more efficient inductive activity. The peptide: gp120 complex was scrutinized with a panel of neutralizing anti-gp120 monoclonal antibodies and CD4 itself, illustrating that peptide binding does not interfere with or obscure the CD4 binding site. Conclusions: Two surfaces of gp120 are considered targets for the development of cross neutralizing antibodies against HIV-1; the CD4 binding site and CD4i epitopes. By implementing novel peptides that allosterically induce the CD4i epitopes we have generated a viral envelope that presents both of these surfaces simultaneously.

    Time:

    Title: Domain Scan Libraries & Profiling Antibodies Associated with Hepatic Viral Disease

    Smadar Neeman and Michael Mordekovich
    Tel Aviv University, Israel

    Biography
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    Biography

    Smadar Neeman and Michael Mordekovich
    Tel Aviv University, Israel

    Smadar Neeman completed her B.Sc. in Biology at the George S. Wise Faculty of Life Sciences, Tel Aviv University in2011 and proceeded with her studies in the Direct Ph.D. Program at the Department of Cell Research and Immunology, Tel Aviv University. Her Ph.D. research focuses on developing a novel approach to profile the antibody response towards Hepatitis C virus in order to understand the details of the humoral response towards cancer caused by viruses. Michael Mordekovich completed his B.Sc. in Biology at the George S. Wise Faculty of Life Sciences, Tel Aviv University at 2015 and proceeded with his M.Sc studies at the Department of Cell Research and Immunology, Tel Aviv University. Michael's research focuses on "Domain Scan" analysis and use of Next Generation Sequencing in profiling the human immune response towards virus infections.



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    Abstract

    Smadar Neeman and Michael Mordekovich
    Tel Aviv University, Israel

    Hepato cellular Carcinoma and Cirrhosis are often the result of viral infections and in particular Hepatitis B and Hepatitis C viruses. The prevalence of these infections is very wide spread and estimated to exceed 300 million people worldwide. The immune response towards these infections can be complex and whereas some individuals deteriorate to malignant disease, others can actually clear the infection. The correlates for effective clearance are not known and could be associated with specific antibodies directed towards the viral antigens. We have developed a novel approach to profile the antibody response towards Hepatitis C virus, and have conducted a pilot study analyzing clinical samples that represent a number of disease situations. Our methodological platform stems from combining three serological methods developed in our lab: Combinatorial diagnostics, Deep-panning and Domain-scan libraries. Here we have developed specific Domain-scan libraries representing epitopes of HCV antigens. These have been screened against HCV positive polyclonal sera. The signature responses toward specific domains will be described and discussed in relation to the clinical status of the HCV infected individuals. Understanding the details of the humoral response towards cancer causing viruses may assist in prognosis on the one hand and better designing therapeutic regimens on the other.

    Time:

    Title: Charged Amino Acid-rich Leucine Zipper-1 (Crlz-1) as a Target of Wnt Signaling Pathway Controls Pre-B Cell Proliferation by Affecting Runx/CBFβ-targeted VpreB and λ5 Genes

    Sung-Kyun Park
    Korea Research Institute of Bioscience and Biotechnology(KRIBB), Republic of Korea

    Biography
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    Biography

    Sung-Kyun Park
    Korea Research Institute of Bioscience and Biotechnology(KRIBB), Republic of Korea

    Sung-Kyun Park received his PhD in Immunology from Kyung Hee University in 2011, working with Prof. Chang-Joong Kang and then worked as a postdoctoral researcher with Drs. William Garrard and Nicholas Conrad at University of Texas Southwestern Medical Center to 2016. He is currently Researcher as a principal investigator of Infectious Disease Research Center at Korea Research Institute of Bioscience and Biotechnology(KRIBB). He has contributed greatly to the understanding of molecular mechanisms in B cell development and function. Now, his work is also focused on finding new mechanism for the regulation of B cell function especially in metabolic syndrome.



    Abstract
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    Abstract

    Sung-Kyun Park
    Korea Research Institute of Bioscience and Biotechnology(KRIBB), Republic of Korea

    The proliferation of pre-B cells is known to increase further the clonal diversity of B cells at the stage of pre-B cells by allowing the same rearranged heavy chains to combine with differently rearranged light chains in a subsequent developmental stage. Crlz-1 (charged amino acid-rich leucine zipper-1) was found to control this proliferation of pre-B cells by working as a Wnt (Wingless-related MMTV integration site) target gene in these cells. Mechanistically, Crlz-1 protein functioned by mobilizing cytoplasmic CBFβ (core binding factor β) into the nucleus to allow Runx (runt related transcription factor)/CBFβ hetero-dimerization. Runx/CBFβ then turned on its target genes such as EBF (early B cell factor), VpreB and λ5 and thereby pre-BCR (pre-B cell receptor) signaling leading to the expression of cyclins D2 and D3. Actually, the proliferative function of Crlz-1 was demonstrated by not only Crlz-1 or β-catenin knock-down but also Crlz-1 overexpression. Furthermore, the mechanistic view that the proliferative function of Crlz-1 is caused by relaying Wnt/β-catenin to pre-BCR signaling pathways through the regulation of Runx/CBFβ hetero-dimerization was also verified by employing niclosamide, XAV939 and LiCl as Wnt inhibitors and activator, respectively.

    Time:

    Title: Combination Therapy of Ultrasound Hyperthermia and Immunostimulant Enhances Systemic Antitumor Immunity for Cancer Tumor Treatment

    Win-Li Lin
    Institute of Biomedical Engineering, Taiwan

    Biography
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    Biography

    Win-Li Lin
    Institute of Biomedical Engineering, Taiwan

    Win-Li Lin received his Ph.D. degree from the University of Arizona, USA, in 1990. He joined the faculty of National Taiwan University in 1992 and became a full professor in 2001. He has been interested in biomedical engineering research, particularly in the area of ultrasound thermal therapy for tumor treatment, blood-brain barrier disruption with focused ultrasound and microbubbles, targeted nano drug delivery with focused ultrasound for central nervous system diseases and tumors, and development of high-power ultrasound devices for medical uses with magnetic resonance imaging guidance. Recently, his research is focused on developing methods to kill the primary tumour, including cancer stem cells, and the metastatic tumours.



    Abstract
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    Abstract

    Win-Li Lin
    Institute of Biomedical Engineering, Taiwan

    Objective: To evaluate whether antitumor immunity is enhanced systemically by combining pulsed-wave ultrasound hyperthermia (pUSHT) and local injection of an immunostimulant, OK-432. Methods: BALB/c mice were inoculated with CT26-luc-GFP tumors on both flanks as a bilateral tumor model. The treated-side tumor underwent a 10-day treatment with pUSHT and/or subcutaneous injection of OK-432. The untreated-side tumor was used to assess the degree of anti-tumor immune response systemically induced by different therapeutics. In a rechallenge tumor model, a rechallenge tumor was implanted contralaterally after the treated-side tumor experienced a 5-day treatment and then surgically removed. This model was designed to evaluate the establishment of a long-term active tumor-specific immune memory for preventing tumor recurrence. Results: The tumor growth rate and growth activity of both treated and untreated tumors were significantly inhibited with the OK+pUSHT combination treatment. Systemic anti-tumor effect seemed to be prolonged. The results of IF and H&E staining showed that there was a remarkable increase of NK cell infiltration in the tumor and an earlier necrosis area for the combination treatment. Survival rates significantly increased for the OK+pUSHT group. In the rechallenge test, the volume of all reimplanted tumors decreased and then disappeared as compared with the control group. Conclusion: Combining pUSHT with local injection of immunostimulant OK-432 for a local tumor treatment may lead to activation of systemic antitumor immunity.

    Time:

    Title: Anca Vasculatis In Algeria

    Gadiri Sabiha
    Clinic St Therese, UHC Annaba, Algeria

    Biography
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    Biography

    Gadiri Sabiha
    Clinic St Therese, UHC Annaba, Algeria

    Dr. Gadiri Sabiha has completed her PhD from Medicine Faculty in Annaba, Algeria and postdoctoral in immunology from Medical Faculty Annaba, Algeria. She is the headmistress of unit of autoimmunity, Clinical Hospital St Therese Annaba, Algeria and a veteran member of the Pasteur Institute Algeria. She is a deputy treasurer of Algerian society of Immunology. She has participated at scientific internationals manifestations in Algeria, Tunisia, Morocco, Italia, Austria, France, Germany.



    Abstract
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    Abstract

    Gadiri Sabiha
    Clinic St Therese, UHC Annaba, Algeria

    Introduction: Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis comprises microscopic polyangiitis (MPA), granulomatosis with polyangiitis (GPA) and eosinophilic GPA (EGPA). Major target antigens of ANCA associated with vasculitis are myeloperoxidase (MPO) and proteinase 3 (PR3). MPO-ANCA is related to MPA and EGPA, and PR3-ANCA is the marker antibody in GPA. Objective: Report the clinical-immunological characteristics of 92 patients with positive ANCA vasculitis Material and methods: 92 patients (64 Female at 28 male ), with ANCA vasculitisaccording to the Chapel Hill classification.ANCA was performed by indirect immunofluorescence, supplemented by immunodot to determine their specificity MPO/PR3. Resultants: The mean age of patients was 51 years, the diagnosis was: 14 cases of GPA, 21 cases of microscopic polyangiitis (MPA), 04cases of EGPA ,53 subjects had signs of overlap between the GPA and MPA. The clinical picture was dominated by renal disease followed by lung disease and rheumatologic signs.Some patients had cardiac involvement. 71 patients had p-ANCA (77,17%), of which 43 were anti-MPO specificity (46.73%), 21 patients had c-ANCA (22.83%), including 9with a specific anti-PR3 (9, 78%), patients showed no 2 searched specificities (44.44%). Conclusion: ANCA vasculitis is rare, clinical and immunological spectrum is very heterogeneous. The demonstration of ANCA directed vis-a-vis PR3 and MPO specific as an aid in the diagnosis of systemic vasculitis

    Time:

    Title: Polymorphism in Exon 2 of CD1a and CD1d Genes in Riyadh (Saudi Arabia) and its Association with Colon Cancer Disease

    Suliman Alomar
    Saudi Arabia

    Biography
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    Biography

    Suliman Alomar
    Saudi Arabia



    Abstract
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    Abstract

    Suliman Alomar
    Saudi Arabia

    CD1 molecules are MHC-like glycoproteins class I implicated in presenting different glycolipids to antigen specific T and NKT cells. Five genes have been identified CD1a, CD1b, CDc, CD1e and CD1d. Few polymorphic sites were reported in these genes and the functional polymorphisms were mapped in exon 2 encoding for the alpha 1 domain. The aim of this study was to investigate the distribution of exon 2 polymorphisms of CD1a and CD1d in Saudi population and their association with colon cancer disease (CC). Typing for the polymorphic sites was performed using PCR-SSP through a standardized protocol. Frequencies of CD1a *01 and CD1a*02 among healthy individuals were 42% and 89% respectively. Those of CD1d *01 and CD1d*02 were 100% and 45% respectively. These results show that frequencies of CD1a *02 (89%) and CD1d *01 (100%) are in the range of the almost reported frequencies worldwide. However, frequencies of CD1a *01 and CD1d *02 are quite larger than all reported frequencies until now. The frequency of CD1a *02 was significantly less frequent in CC patients (58.6%) (OR = 0.17; CI = 0.079-0.38 and P < 0.0001). The homozygotes CD1a *02/*02 were also less frequent in CC patients (40%) than in controls (58%) (OR=0.48; CI = 0.25-0.89 and P = 0.028). The CD1d*02 allele occurs less frequently in CC individuals (14%) compared to controls (OR=0.48; CI = 0.25-0.89 and P<0.00011). These results show potential protective effect of CD1a*01 and CD1d *02 gene against colon cancer disease in Saudi population.

    Time:

    Title: Cytokine Balance to Plasmodium vivax Infection in a Gold-Mining Area from Amazon Region

    Ricardo Luiz Dantas Machado
    Federal Fluminense University, Brazil

    Biography
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    Biography

    Ricardo Luiz Dantas Machado
    Federal Fluminense University, Brazil

    Ricardo Luiz DantasMachado, Ph. D. is a Full Researcher at Malaria Immunogenetics Laboratory of the Evandro Chagas Institute, Brazilian Ministry of Health. He received his degree in Pharmacisty from Universidade Federal Fluminense, Niteroi, Brazil in 1984 and his Ph.D. in Parasitology from Universidade Federal do Para, Belem, Brazil in 2001. He is an Associate Editor of the BMC Infectious Diseases, and serves on the editorial board of ISRN-AIDS and World Journal of Clinical Infectious Diseases. His main fields of research are coccidian diagnosis, molecular epidemiology and host-parasite relationship. He has published several scientific peer-reviewed papers, reviews and book chapters.



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    Abstract

    Ricardo Luiz Dantas Machado
    Federal Fluminense University, Brazil

    Background: Malaria is the most devastating protozoan disease afflicting humans. The most widespread human malaria parasite, causes 130-390 million clinical episodes. Although the pathophysiology of vivax malaria remains poorly understood. The cytokines was reported to be of importance in human malaria include TNF-α, IL-6 and IL-10, but the mechanisms by which humans regulate pro- and anti-inflammatory responses on exposure to different malaria parasites remains unclear. Materials and Methods: We aimed to investigate participation of the cytokines in the immune response to P. vivax infection in a gold-mining area. The serum cytokine levels was assumed from 50 malaria patients and 79 healthy individuals of Itaituba, municipality situated on southwest of Para state. The plasmatic cytokines IL-2, IL-4 IL-6, IL-10, TNF-α and IFN-γ were quantified by BD Human Th1/Th2 cytokine Kit II and all purchased from BD Biosciences Pharmingen. The statistical analyses were carried out using the Graph-Pad Prism software, version 6.0 and the existence of association was determined by Mann-Whitney test, with level of significance of 0.05. Results: Data analysis indicated significant increase in the TNF-α, INF-γ, IL-6 and IL-10 plasmatic levels (3,54 pg/mL(+/-)3,99; 13,80 pg/mL(+/-)41,52; 217,62 pg/mL(+/-) 534,91; 1.030,44 pg/mL(+/-)2.290,77, respectively) in malaria group as compared with endemic control group (1,86 pg/mL(+/-) 2,67; 4,48 pg/mL(+/-)17,93; 9,67 pg/mL(+/-)16,69; 2,22 pg/mL(+/-)5,20, respectively); no significant differences were detected in the IL-2 and IL-4 plasmatic levels between the groups. Conclusions: Cytokine responses reflect different host strategies for controlling infection in different endemic areas. Our findings showed significant differences in TNF-α, INF-γ, IL-6 and IL-10 levels produced in association with parasite burden, which itself is related to the clinical course. However, the cytokine balance needs to be evaluating in different areas and population.

    Time:

    Title: Immunomodulatory Effects of Anti-Tumor Necrosis Factor α: Relationships with Behcet disease clinical characteristics

    Djamel Messaoudene
    University of Boumerdes, Algeria

    Biography
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    Biography

    Djamel Messaoudene
    University of Boumerdes, Algeria

    Dr. Messaoudene Djamel chief Department of Biology, Faculty of Sciences, University of Boumerdes (UMBB), Senior Research Fellow at the Laboratory of Cellular and Molecular Biology (LBCM), Cytokines and NO-synthase team, University of Sciences and Technology Houari Boumedien, Algeria.



    Abstract
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    Abstract

    Djamel Messaoudene
    University of Boumerdes, Algeria

    Objectives: To investigated The Th1 cytokines and nitric oxide production in different types of manifestations of Behcet disease and the effect of anti-TNFα treatment on IL12 and NO induction in PBMC from Algerian patients with BD. Methods: Peripheral venous blood was drawn from 93 patients with different type of manifestation of Behcet disease and from 63 controls. Cytokine concentration was measured by ELISA and NO levels were assessed by modified Griess's method. Cells were cultured with or without anti-TNF-α. IL-12 levels were measured by specific enzyme-linked immunosorbent assay. Nitric oxide levels were evaluated using a modified Griess method. Results: Our results showed that patients with active disease had significant elevation of IL-12 and NO concentrations compared with controls. Cytokine and NO production profiles are specific to the clinical manifestation. Treatment with anti-TNF α did not reduce significantly the number of PBMC secreting IL12 in all type of manifestation studied. Further, anti-TNF-α induced significantly reduced production of NO in cell culture supernatants; a favorable clinical response to anti-TNF α was associated with Uveits and Neurobehcet manifestations. We observed that cytokine and NO production profiles are specific to the clinical manifestation, this specificity suggests the involvement of different specific T cell populations in the regulation of immune responses occurring during active Behcet disease. These cells are probably specific to local auto-antigens. A single infusion of anti-TNF significantly did not reduce the number of PBMC secreting IL12 in all type of manifestation studied. anti-TNFα treatment induced a significant decrease the levels of nitric oxide production this modulation was specific to the clinical profile , a favorable clinical response to anti-TNF α was associated with Uveits and Neurobehcet manifestations Conclusion: These results suggest the implication of the IL12 and nitric oxide in physiopathology of BD. Our findings indicate that TNF- α plays a pivotal role in BD, and that anti-TNF- α therapy reduces NO production and may play a protective role against inflammation specially in uveites and neurobehcet manifestations.

    Time:

    Title: Reduced central serotonin up-regulates prostaglandin E2 production in the anteroventral preoptic region during systemic inflammation

    Luiz G. S. Branco
    University of Sao Paulo, Brazil

    Biography
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    Biography

    Luiz G. S. Branco
    University of Sao Paulo, Brazil



    Abstract
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    Abstract

    Luiz G. S. Branco
    University of Sao Paulo, Brazil

    Serotonin (5-HT) is a neuromodulator involved in several central-mediated mechanisms, such as endocrine processes, behavior and sleep. Dysfunction of the serotonergic system is mainly linked to psychiatric disorders, but emerging evidence suggests that immune system activation may also alter brain 5-HT signaling. However, whether central 5-HT modulates systemic inflammation (SI) remains unknown. Thus, we measured 5-HT and its metabolite 5-hydroxyindole-3-acetic acid (5-HIAA) in the anteroventral preoptic region [AVPO - the hierarchically most important region for body temperature (Tb) control] during lipopolysaccharide (LPS)-induced SI. We also combined LPS treatment with intracerebroventricular (icv) injection of 5-HT and measured Tb ("hallmark" of SI), AVPO PGE2 (an essential mediator of fever) and PGD2 (a cryogenic mediator), plasma corticosterone (CORT - a stress marker with an endogenous anti-inflammatory effect) and IL-6 (an immune mediator) levels. We also assessed tail skin temperature [used to calculate heat loss index (HLI)] to assess a key thermo effector mechanism. As expected we observed LPS-induced increases in Tb, AVPO PGE2 (whereas PGD2 remained unchanged), plasma CORT and IL-6 levels, as well as a decrease in HLI. These changes were accompanied by reduced levels of AVPO 5-HT and 5-HIAA. Besides we also observed negative correlations between 5-HT and 5-HIAA with plasma CORT levels and Tb, respectively. Moreover, icv 5-HT microinjection caused a U-shaped dose-response curve in LPS fever, in which the intermediate dose reduced the febrile response. Icv 5-HT microinjection prevented the LPS-induced increases in AVPO PGE2 (whereas did not alter PGD2), plasma CORT and IL-6 levels; besides preventing the reduced HLI. Our data are consistent with the notion that the AVPO 5-HT synthesis is down-regulated during SI favoring AVPO PGE2 synthesis and consequently potentiating the immune response. These results reveal a novel effect of central 5-HT as an anti-inflammatory neuromodulator that may take place during psychiatric disorders treatment with 5-HT reuptake inhibitors besides suggesting that 5-HT modulation per se is a potential therapeutic approach for inflammatory diseases.

    Time:

    Title: Type 1 Diabetes and Coeliac Disease in Algeria

    Meriche Hacene
    Clinic St Therese, UHC Annaba, Algeria

    Biography
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    Biography

    Meriche Hacene
    Clinic St Therese, UHC Annaba, Algeria



    Abstract
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    Abstract

    Meriche Hacene
    Clinic St Therese, UHC Annaba, Algeria

    Introduction : The co-occurrence of celiac disease and type 1 diabetes has been reported as 5-7 times more prevalent than celiac disease alone. The clinical presentation of celiac disease in patients with type 1 diabetes may vary considerably. Less than 10% of patients with type 1 diabetes and celiac disease show gastrointestinal symptoms. Celiac disease is more prevalent in type 1 diabetic patients than in the general population in Algeria country. As follows the ESPGHAN guidelines, diagnosis of celiac disease is based on the presence of villous atrophy and crypt hyperplasia by intestinal biopsy and the presence of antibodies against tissue transglutaminase. Material and methods : In a total of 420 diabetic adults were screened for coeliac disease by simultaneous detection of human IgA isotype antibodies directed against tissue transglutaminase, gliadin and deaminated peptide of gliadin by FIDIS Celiac DPG kits (Theradiag). Resultants: Forty diabetic adults were positive for IgA class transglutaminase and a Deaminated Peptide of Gliadin antibody, all underwent biopsy of the small intestine. Twenty two cases of coeliac disease were found; all of these adults had characteristic biopsy establishing partial or total villousatrophy. Conclusion: It was concluded that IgA class transglutaminase and deaminated peptide of gliadin antibody were a good marker of coeliac disease for screening tests of high risk populations. The prevalence of coeliac disease in Algerian diabetic population was 5.2% and we suggest that diabetic adults be screened routinely for antibody for coeliac disease at diagnosis of type 1 diabetes, every year in the first five years of follow-up.

    Time:

    Title: Bcl-2 inhibitor ABT-737 alleviatedin vivo and in vitroallergic rhinitis reactions

    Hee-Yun Kim
    Kyung Hee University, Republic of Korea

    Biography
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    Biography

    Hee-Yun Kim
    Kyung Hee University, Republic of Korea

    Hee-Yun Kim was born in 1985 and received M.S. degree in Biological Engineering from Inha University, R.Korea. Currently, He is a Ph.D. candidate at Kyung Hee University, R. Korea. He has been published many articles about allergic inflammation. He won an Excellent Research Paper Award from Kyung Hee University in 2017.



    Abstract
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    Abstract

    Hee-Yun Kim
    Kyung Hee University, Republic of Korea

    ABT-737 is an inhibitor of Bcl-2 and has an anti-cancer property. Recent studies reported that tumor growth, invasion, angiogenesis, and metastasis were accelerated by inflammatory reactions. Here the aim of this study is to assess the anti-allergic inflammatory effect of an anticancer agent, ABT-737 on human mast cell line HMC-1 and allergic rhinitis (AR) animal model. ABT-737 significantly diminished production and mRNA expression of pro-inflammatory cytokines on activated human mast cell line, HMC-1. In an AR animal model, ABT-737 decreased rub scoring and IgE, histamine, thymic stromal lymphopoietin, pro-inflammatory cytokines, and vascular endothelial growth factor levels from the serum of ovalbumin-challenged mice. ABT-737 reduced numbers of infiltrated mast cells and eosinophils in nasal mucosa tissues of AR mice. In addition, levels of Th2 cytokines and chemokines were significantly reduced by ABT-737 in nasal mucosa tissues of AR mice. In conclusion, the results suggest that ABT-737 is potential candidate for treatment of AR.

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