International Conference on Innate Immunity July 20-21, 2015 Barcelona, Spain

Biography:

Dr. Deshane is a pulmonary immunologist with expertise in immune regulation in asthma. She investigates Myeloid-Derived Regulatory Cell biology and free radical mechanisms that regulate their differentiation and function. She pioneered these investigations both in mouse models and human asthma. Dr. Deshane has authored 46 peer-reviewed publications, including high impact journals like Journal of Experimental Medicine, Journal of Clinical Investigations, Journal of Allergy and Clinical Immunology, Immunity and Cancer Research. She serves on the editorial boards for the journals Allergy and American Journal of Respiratory Cell and Molecular Biology and serves on grant review committees. Dr. Deshane is a Parker B Francis Fellow and funded by FAMRI and NIH.

Abstract:

This lecture will address the expanding role for macrophages and their plasticity highlighting their potent inflammatory and immunoregulatory activities in chronic lung diseases, specifically asthma. The intriguing role played by environmental exposures that regulate their plasticity, both in differentiation and function of these immature myeloid cells will be discussed. Important insights will be shared regarding how proportions and functions of subsets of regulatory myeloid cells can discriminate asthma from chronic obstructive pulmonary disease. In addition, this lecture will discuss new paradigms on pathogenesis of asthma based on a major role for myeloid-derived regulatory cells as regulators of balance between immune tolerance and inflammation by eliciting a pathologic immune/inflammatory response that represents a novel form of autoimmunity.

Biography:

Biography: Dr. Diehl is a senior pathologist and group leader at Genentech. She has more than 10 years of drug development experience in the area of immunologically mediated disease, especially inflammatory bowel disease. Her research interest is the role of the innate immune system in maintenance of intestinal mucosal homeostasis.

Abstract:

Dysfunction of the mucosal immune system leading to inappropriate recognition of commensal bacteria plays a central role in development of inflammatory bowel disease. Dendritic cells (DCs) are emerging as critical mediators of immune homeostasis through selective induction of immune responses. DCs form an extensive network in the intestinal lamina propria, project transepithelial dendrities to sample the luminal environment, and deliver antigens to mesenteric lymph nodes to induce either tolerance or immune response. While DCs are recognized as critical in maintaining mucosal homeostasis, the mechanisms by which they fulfill this role have not been fully elucidated. The role of CD83 homotypic interactions in DC regulation and other emerging mechanisms will be reviewed.

Biography:

Jean-François Augusto is Associate Professor of Nephrology in Angers University Hospital, France. He has studied Innate Immunity and has completed his PhD from Angers University, France, in April 2015. He has expertise in Clinical Nephrology, including auto-immune and systemic diseases, and Critical Care Medicine. His main interest is the study of innate immunity and especially pattern recognition receptor biology and their implication in pathophysiology of systemic and auto-immune diseases.

Abstract:

Antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) are a group of human life-threatening diseases characterized by multiorgan involvement. AAV diagnosis relies on the histological identification of small vessel vasculitis in an affected organ and on the identification of ANCA directed to myeloperoxidase (MPO) or proteinase 3 (PR3). ANCA detection allows a rapid diagnosis and the initiation of immunosuppressive treatments. However, up to 15% of affected patients are ANCA negatives, which frequently delays the treatment initiation. Pentraxin 3 (PTX3), such as MPO and PR3, is stored in human neutrophil granules and is expressed on apoptotic neutrophil surface. We therefore investigated the presence of anti-PTX3 autoantibodies (aAbs) in the sera of AAV patients, to evaluate the potential interest of this novel biological marker in the diagnosis of AAV. Presence of anti-PTX3 autoantibodies was analyzed by a specific ELISA in sera from 150 AAV patients and in sera of 227 healthy subjects (HS). Using indirect immunofluorescence on human fixed neutrophils, we also analyzed the staining pattern associated with the presence of anti-PTX3 aAbs. Anti-PTX3 aAbs were detected in 56 of 150 (37.3%) of the AAV patients (versus 12 of 227 (5.3%) of HS, p<0.001) and, interestingly, in 7 of 14 MPO and PR3 ANCA negative AAV patients. Moreover, by indirect immunofluorescence on fixed neutrophils, anti-PTX3 aAbs gave rise to a specific cytoplasmic fluorescence pattern distinct from the classical cytoplasmic (c-ANCA), perinuclear (p-ANCA), and atypical (a-ANCA) pattern. No association between anti-PTX3 aAb titers and disease activity was found. Anti-PTX3 aAbs appear thus as a promising novel biomarker in the diagnosis of AAV, especially in patients without detectable MPO and PR3 ANCA.

Biography:

Ester Boix defended her PhD at the Universitat Autònoma de Barcelona (Spain) and spent 5 years postdoctoral studies at the National Institutes of Health, Bethesda (USA) and Structural Biology Unit, University of Bath (UK). She has been awarded a Ramon y Cajal senior researcher contract in 2002. She is currently an Associate Professor at the Dpt. of Biochemistry and Molecular Biology at the Universitat Autònoma de Barcelona and principal investigator of the research group on Host defense ribonucleases. She has published more than 60 papers in peer-reviewed journals; her main interest focusing on the mechanism of action of antimicrobial RNases.

Abstract:

Human secretory RNases are wide-spectrum host defense proteins. They are secreted by innate cell types upon infection and constitute a first line immune barrier. Our research group is exploring their mechanism of action at distinct cellular levels. In this work we compare the three main human antimicrobial RNases: RNase 3 specifically secreted by eosinophils, RNase 6, expressed by neutrophils and monocytes, and RNase 7 predominant in keratinocytes. By applying site directed mutagenesis and peptide synthesis we have identified the main structural determinants for the proteins’ cytotoxicity on several Gram negative and Gram positive bacteria species together with Candida albicans yeast. Domains responsible for lipopolysaccharide binding, cell agglutination and membrane destabilization have been located at the protein N-terminus. The identified antimicrobial motives served as a template to design antimicrobial peptides. Protein derived peptides were engineered reproducing efficiently the parental protein antimicrobial properties. Moreover, together with an unspecific membrane lysis killing mechanism, the studied RNases were able to internalize at sublethal concentrations, blocking the cell viability and potentially targeting the cellular nucleic acids. We can conclude that human antimicrobial RNases work as host multitask proteins contributing to the clearing of the infection focus. Complementary, human RNases can also serve as templates towards a structure- based drug design of novel antimicrobial agents. In particular, potential contribution of the enzymatic activity in the RNases cytotoxicity envisages cellular RNA targeting as an effective strategy for alternative antibiotic development.

Biography:

Abstract:

Objective : To evaluate the ability of the soluble vascular endothelial growth factor receptor (sFlt-1), neutrophil-flt-1, monocyte-flt-1, pentraxin3 (PTX3), nitric oxide (NO) and alpha fetoprotein (AFP) measurements at gestational weeks 14-18 to predict preeclampsia (PE).
Subjects & Methods: Fifty pregnant females at second trimester of pregnancy divided into 25 normotensive pregnant females who remained normotensive till delivery (group I) and 25 high risk pregnant females who subsequently developed PE (group II). Twenty five healthy non-pregnant females served as control (group III). Maternal blood samples were collected at 14-18 gestational weeks. EDTA samples were investigated for both neutrophil- and monocyte-flt-1 by flowcytometer. Stored serum samples were analyzed for sFlt-1, PTX3, NO and AFP by ELISA.
Results: Alpha fetoprotein, sflt-1 and pentraxin 3 were found to be statistically significantly increased in group II when compared with group I (P-value = 0.024, < 0.001 & 0.006) and group III (P-value = < 0.001). However, there was statistically significant decrease in neutrophil-flt-1 and nitric oxide in group II when compared with group I (P-value = < 0.001 & 0.016). Group II had significant negative correlation between soluble flt-1 and both neutrophil- & monocyte-flt-1 (P-value = Ë‚ 0.001 & 0.009) and between neutrophil-flt-1 and PTX3 (P-value = 0.007). Soluble flt-1 was found to have the highest predictive value for predicting preeclampsia (AUC = 0.941& P-value = < 0.001)
Conclusion: Soluble flt-1 was the best single biomarker to predict preeclampsia at second trimester of pregnancy with the best diagnostic sensitivity and specificity.

Biography:

Sung Su Yea has completed his PhD from Korea Advanced Institute of Science and Technology on 2000.Since 2001, he has been working as a professor of Dept. of Biochemistry,Inje University College of Medicine, South Korea. He had been working as a visiting scholar at Michigan State University (1997-1998) and University of California, Irvine (2011-2013), USA.He has published more than 64 papers in reputed journals, 29 patents (including patents pending) and has been serving as an editorial board member of repute.

Abstract:

Phosphoinositide 3-kinase (PI3K) and mechanistic target of rapamycin (mTOR) play fundamental roles in signal transduction for cell proliferation and survival. Recently, specific inhibitors of PI3K isoforms are being evaluated for their therapeutic potential in cancer. However, little is known about their roles in natural killer (NK) cell, an effector lymphocyte of innate immunity. Here we assessed how different classes of PI3K inhibitors and mTOR complex (mTORC) inhibitors affect the function of NK cells. Inhibitors of all class I isoforms (pan-PI3K) significantly impaired cell-mediated cytotoxicity and antibody-dependent cellular cytotoxicity of NK cells against tumor cells, whereas isoform-selective inhibitors had little effect; in particular, no significant effect was observed in NK cells treated with p110a-selective inhibitors. Production of cytokines and chemokines including IFN-g in NK cells stimulated through NKG2D and NK1.1 was blocked by a pan-PI3K inhibitor and partially reduced by a p110d inhibitor, with lesser effects of p110a inhibitors. NK cell-mediated cytotoxicity against tumor cells as well as IFN-g production through NKG2D were down-regulated by PP242, an inhibitor for both complex of mTOR, but not by rapamycin inhibiting mTORC1 only. In anti-NKG2D antibody-stimulated NK cells, pan-PI3K inhibitor decreased the phosphorylation of AKT and ERK1/2 phosphorylation, while p110a inhibition modestly reduced PI3K signaling output as measured by AKT and ERK1/2 phosphorylation. These results reveal the role of PI3K isoforms and mTOR complexes in NK cell functions and indicate that selective p110a inhibitors would provide a better therapeutic window for specific disease states than achieved by targeting all isoforms.

Biography:

Carl E I Janssen has completed his PhD at the age of 27 years from KU Leuven and published 6 papers in reputed journals. He was also involved in business plan writing for a university spin-off.

Abstract:

Granulomas are one of the diagnostic features of Crohn’s disease(CD). Genetic variants in nucleotide oligomerisation domain 2(NOD2) are linked with CD. We reported granulomas-in-follicles (GIF) are linked to increased IFNγ/IL1β/IL17/IL23R/RIP2 expression, polycyclic granulomas and extended disease to anus, appendix, lymph nodes or mouth in paediatric CD(pCD). We selected 10pCD cases with granulomatous appendicitis (pCD-A) and screened all available tissue for granulomas in intestinal lymph nodes. We studied granulomas by a standardized set of morphological features and immunohistochemistry; CD68 to detect microgranulomas, CD20 to visualize GIF, cytokines TNFα and IL17, and determined NOD2 variants p.R702W(rs2066844), p.G908R(rs2066845) and p.Leu1007fsX1008(rs2066847). At least one variant was present in 60% of pCD-A. Lymphocyte emperipolesis was observed in 60% of pCD-A and found in polycyclic granulomas irrespective of NOD2 variants, GIF or lymph node involvement. rs2066847 (30%), was not associated with GIF or lymph node involvement. rs2066845 was found in a single case with GIF, but without lymph node granulomas. rs2066844 (20%) was associated with GIF and lymph node involvement. All except one case exhibited tissue sclerosis. Polycyclic granulomas and eosinophils were common in NOD2+, but virtually absent in NOD2- cases. Coronary CD68+ granulomas, CD20+ GIF and lymph node involvement were prominent in NOD2-, but rare in NOD2+ cases. No significant difference in TNFα or IL17 staining was related to NOD2 variants, GIF or lymph node granulomas. This is the first pathological study of pCD-A granulomas. Although NOD2 variants were present in the majority of cases, they were independent of GIF, a novel feature linked to intestinal lymph node involvement.

Biography:

Wolfgang W Leitner is the Chief of the Innate Immunity Section, NIAID/NIH. He was involved in deciphering the mechanisms underlying the regeneration of splenic autotransplants and developed the first nucleic acid vaccine for P. berghei malaria. While establishing a replicase-based DNA vaccine for the treatment of melanoma, he uncovered the immune mechanism underlying the superior immunogenicity of aphavirus-based nucleic acid vaccines. He has authored more than 70 papers in the areas of vaccine research, basic immunology and cancer therapy. He joined the NIAID Extramural Program as a Program Officer in 2008 and oversees the innate immunity portfolio, including vaccine adjuvant research.

Abstract:

This lecture will guide the audience through the process of research funding by the US National Institutes of Health. The extramural program of the NIH provides approximately 1/3 of biomedical research funding in the US and also support numerous research projects overseas. Of the 27 NIH institutes, the NIAID is one of the two largest and responsible for research on infectious diseases, transplantation, various immune-mediated diseases as well as basic immunology. In addition to research on vaccines, the NIAID conducts and supports extensive research on vaccine adjuvants, immune mechanisms of protection, and the mechanism of action of adjuvant. The main funding mechanisms for pre-clinical research are the R01 research grant and the R21 exploratory grant for high risk/high reward research proposals. For most funding announcements, applications are accepted from non-US institutions and non-US citizens. To assist extramural investigators further, the NIAID provides numerous resources such as the tetramer core facility, BEI repository of biological reagents, computational resources, or the immune epitope database. The NIH Program Officer assigned to a specific research topic is the applicant’s primary point of contact and can help guide the applicant through the application, award and post-award process.

Biography:

Dr. Litvak, assistant professor at UMMS, has studied immunology, metabolism and systems biology for 15+years and published his research papers in high-profile peer-reviewed journals such as Nature, Nature Immunology, Nature Cell Biology and Molecular Cell. He is an editor for the Immunome Research Journal. Dr. Litvak is a member of the Educational Resource Cluster at UMass Center for Microbiome Research. He also serves on the review committee for the National Center for Complementary and Alternative Medicine (NCCAM/NIH).

Abstract:

This lecture will introduce the emerging field of immunometabolism and will cover a range of topics addressing the role of metabolic networks in the regulation of antiviral immunity. The lecture will emphasize the function of central metabolic pathways in the epigenetic reprogramming of innate antiviral immunity and will discuss its contribution to the balance of beneficial effects and deleterious sequelae of the antiviral response. In addition, this lecture will present a variety of systems biology approaches and will highlight their importance as a powerful tool in the analysis of complex immune-metabolic interactions. Finaly, attendees of this lecture will be familiarized with an application of the systems biology approach to the discovery of new drug targets for the therapeutic control of viral infections or autoimmune disease.

Biography:

Professor Bernhagen studied Biochemistry and Immunology at the University of Tübingen, Germany, and at Queen Mary College, London, UK. He performed a sandwich PhD thesis at the University of Tübingen and at the Picower Institute for Medical Research, Manhasset, NY, USA, and was trained as a postdoc at the Picower. Professor Bernhagen currently is a Full Professor of Biochemistry and Molecular Cell Biology at RWTH Aachen University, Germany, and is the Chair and Director of the homonymous institute. His main research interest has been on cytokines, chemokines and their role in inflammation, with a focus on MIF and the biochemical and structural features and mechanisms of such inflammatory mediators. He also studies the COP9 signalosome. Studied disease models encompass rodent model of atherosclerosis, sepsis, liver and kidney disease as well as colitis and colorectal cancer. Professor Bernhagen has authored more than 120 peer-reviewed papers in these areas, several of them published in leading journals such as Nature, Nature Medicine, or PNAS. He has serves on the editorial board of several journals and serves on several review committees for extramural funding and various fellowship organizations.

Abstract:

Inflammatory processes such as those promoting atherosclerotic lesion formation are pivotely driven components of the innate and adaptive immune axis. Chemokines and their receptors are a particularly prominent part of the innate immune arm. While the role of classical chemokines, i.e. belonging to the CC or CXC families, is increasingly well understood, it also has become clear that the underlying ligand/receptor system is characterized by a previously unanticipated complexity of cross-reactivities and homo- and heteromerization events. Moreover, an emerging family of chemokine-like inflammatory mediators termed ‘innate chemokines’, CLF chemokines or micro-chemokines, which additionally struc¬turally and functionally overlaps with the mediator class of alarmins has been identified to modulate inflammatory reactions in the atherogenic arterial wall but also numerous other inflamed tissues. Innate or CLF chemokines share functional homology with classical chemokines and signal through classical chemokine receptors, whereas they do not exhibit conserved structural features such as N-terminal tandem cysteine residues or the chemokine fold. This lecture will address the molecular basis of target cell activity and the pathophysiological role of several ‘innate chemokines’. Examples will encompass high mobility group binding protein-1 (HMGB1), macrophage migration inhibitory factor (MIF), and certain -defensins. Receptor usage, signaling, innate immune cell regulation, and involvement in various inflammatory conditions, including atherosclerosis will be discussed. Finally, the lecture will outline potential strategies to specifically and thera¬peutically target such mediators either in conjunction or explicit exclusion of the co-targeting of classical chemokines.

Biography:

Dr Anwen Siân Williams completed her PhD at the age of 25 years from the University of Wales Institute of Science and Technology and postdoctoral studies from Cardiff University. She is a pharmacist and senior member of the academic staff at Cardiff University’s School of Medicine. Dr Williams is a biomedical research expert who has published over 60 papers in reputed journals. She leads a successful scientific research programme within the Institute of Infection and Immunity that is aimed at delivering excellent teaching and learning opportunities for undergraduate and postgraduate students that is centred upon the study of arthritis.

Abstract:

The cellular and molecular signals that safeguard the architecture of the joint during an acute flare of inflammatory arthritis are ill defined. Published data from our group clearly identifies interleukin-6 (IL-6) signaling pathway as important factors that alter early inflammation, tissue homeostasis and tissue damage (1-3). We use relevant cell-based in vitro assays and in vivo models to assign specific IL-6 mediated molecular mechanisms that regulate degenerative cell functionality. We also explore the potential value of a pertinent IL-6-directed antagonist as a preventative therapy for early joint injury during experimental inflammatory arthritis. The manner by which the IL-6 pathway regulates cell trafficking during arthritis is characterized and its impact upon bone homeostasis is assessed.

Biography:

Bhattacharyya received his Ph.D. in Plant Science from the University of Western Ontario, Canada. Following his graduate studies, he joined John Innes Institute, England for his postdoctoral research and isolated the rugosus locus studied by Gregor Mendel. His group has been engaged in conducting research in the area of plant disease resistance with a goal to enhance broad-spectrum disease resistance in soybean. Currently, he directs a multiinstitutional research project funded by USDA-NIFA. He has published over 60 scientif papers mostly in high profile journals. He serves several journals including BMC Plant Biology, BMC Genomics, Molecular Biotechnology, Frontiers in Agricultural Biological Chemistry, and Journal of Plant Genome Sciences for editorial duties.

Abstract:

We are surrounded by innumerable number of pathogenic organisms. Fortunately, we are infected by only a few organisms. Crop plants also encounter a large number of microorganisms on a daily basis; only a few of which are pathogenic. A crop plant has the ability to defend pathogens of all other crop species due to their nonhost immunity mechanisms. For example, soybean is immune to maize pathogens; whereas, maize is immune to soybean pathogens. Nonhost resistance mechanisms are broad-spectrum and durable. Therefore, utilization of nonhost resistance mechanisms has been considered to be ideal for enhancing disease resistance in crop plants. We tested this hypothesis by identifying and then transferring Arabidopsis nonhost resistance genes to soybean. We selected two soybean pathogens: the oomycete pathogen, Phytophthora sojae, and the fungal pathogen, Fusarium virguliforme, for this study. Both are serious soybean pathogens. Together, they can cause soybean yield suppression valued up to half-a-billion US dollars. We have isolated 30 putative P. sojae-susceptible (pss) Arabidopsis mutants. Among 30 pss mutants, 14 were also susceptible to F. virguliforme. We have cloned five Arabidopsis nonhost resistance genes by utilizing six of these 14 selected pss mutants. We have transferred two of these genes encoding a glycine-rich protein and a folate transporter to soybean. Transgenic soybean plants carrying these genes are resistant to both P. sojae and F. virguliforme. Thus, our results confirm the applicability of nonhost resistance mechanisms for creating broad-spectrum disease resistance in crop plants. We have also demonstrated that folate is essential for nonhost immunity

Biography:

Prof Middleton completed his PhD at Lancater University and postdoc research at Cambridge and Bath before working as Senior Scientist in inflammation biology with Novartis (Vienna). He obtained an academic position in Keele University where he became Senior Lecturer, Reader and Professor of Immunology. Currently he is Professor and Reader of Immunology at the University of Bristol. Prof Middleton was a Visiting Professor at CNRS, Toulouse, and has acted as consultant for GSK and biotech industry. He is on the editorial board for Arthritis Research and Therapy and has published in Cell, J Exp Med, Nature Immunol, and J Immunol.

Abstract:

Chemokines are involved in driving leukocyte migration into inflamed tissue. They achieve this by being presented to blood leukocytes by heparan sulphate proteoglycans (HSPGs) on the luminal surface of vascular endothelial cells. We have found that in the synovial endothelial cells of rheumatoid arthritis patients there is induction of a CXCL8 binding site on the HSPG syndecan-3. This suggests involvement of syndecan-3 in leukocyte trafficking into the synovium. Indeed we have shown that leukocyte accumulation and cartilage damage is reduced in syndecan-3 null mice with antigen-induced arthritis. Addition of soluble syndecan-3 in vitro binds chemokines CCL2 and CCL7, and redcues chemotactic responses of moncytes to these chemokines. Injection of soluble syndecan-3 reduces leukocyte accumulation and arthritis severity in antigen-induced arthritis. HSPGs interact with basic residues in chemokines. Therefore addition of competing peptides containing these residues should be inhibitory. Indeed we have found some chemokine peptides do inhibit chemokine-HSPG interaction. These peptides bind HS and inhibit chemokine-driven migration of neutrophils across brain microvascular endothelial cells in vitro. Furthermore these chemokine peptides reduce the swelling of joints of mice with antigen-induced arthritis. In conclusion targeting chemokine-HSPG interactions by adding competing soluble HSPGs (syndecans) and chemokine peptides have therapeutic effects and represents a novel therapeutic approach to inhibit innate immune cell trafficking.

Biography:

Dr Cécile Oury, PhD in Biology, has studied platelet biology for 15 years. In 2001, she was the laureate of the prize Boerhinger Ingelheim for her research on Thrombosis and Haemostasis. She is now Research Associate at the Belgium Fund for Scientific Research, and she is the Head of the Laboratory of Thrombosis and Haemostasis, part of the Unit GIGA-Cardiovascular Sciences at the University of Liège, Belgium. GIGA is an interdisciplinary institute comprising >250 scientists active in biomedicine. Dr Oury’s research focuses on the elucidation of the mechanisms of thrombosis using in vitro studies and animal models. She has a h-index of 18, more than 50 international peer-reviewed papers and 1434 citations. Dr Oury is a Council member of the Belgian Society on Thrombosis and Haemostasis and a member of the International Society on Thrombosis and Haemostasis

Abstract:

This lecture will present the latest findings on the contribution of innate immune cells in thrombosis. It will also address the recent view of platelets as rapid first-line immune responders. Focus will be made on the role of P2X1 receptors for extracellular ATP. It has long been recognized that inflammation shifts the hemostatic mechanisms in favor of thrombosis. Upon tissue damage or infection, a sudden increase of extracellular ATP occurs, that might contribute to the crosstalk between inflammation and thrombosis. On platelets, P2X1 receptors act to amplify platelet activation and aggregation induced by other platelet agonists. These receptors critically contribute to thrombus stability in small arteries. Besides platelets, studies by our group indicate that these receptors are expressed by neutrophils. They promote neutrophil chemotaxis, both in vitro and in vivo. In a laser-induced injury mouse model of thrombosis, it appears that neutrophils are required to initiate thrombus formation and coagulation activation on inflamed arteriolar endothelia. In this model, by using P2X1-/- mice, we recently showed that P2X1 receptors, expressed on platelets and neutrophils, play a key role in thrombus growth and fibrin generation. Taken together, these data suggest that P2X1 receptors are involved in the interplay between platelets and neutrophils. Activation of these receptors by ATP on neutrophils and platelets might be involved in the regulation of inflammation, immunity and thrombosis.

Biography:

Alejandra Pera performed her PhD studies at the Ramón y Cajal University Hospital (Madrid) and at the Università degli Studi of Milan, in 2009. Ever since, she has foccused her work on immunosenescence, particularly on the effect of CMV and age on NK and T cells’ phenotype and function. She has authored several works regarding this topic this year. As well, she has colaborated recently with Dr. Larbi at the Singapore Immunology Network and currently has a Juan de la Cierva postdoctoral contract (Ministry of Science and innovation).

Abstract:

The main topic of this lecture will be based on the current knowledge on age-associated phenotypic and functional changes in NK cells and the role of persistent CMV infection. It will be disclosed the key role of NK cells in the innate immune response against virus infection and tumors. Besides, attendees of this lecture will be familiarized with NK cell subpopulations based on CD56 and CD16 markers expression and the NK cell compartment remodeling in the elderly. As well, it will be shown how age and CMV infection have an effect on the expression of CD57, CD94/NKG2C, activating natural cytotoxicity receptors (NCRs, NKp30, NKp46) and DNAM-1. In summary it will be disscused how NK cell subsets and their phenotype in the elderly are afected not only by age but also by exposure to CMV and the relevance of including the determination of CMV serostatus in those studies addressed to analyze the effect of age on NK cell phenotype and function.

Biography:

Professor Cheol-Heui YUN completed his Ph. D. at the University of Saskatchewan, Canada in the area of immune modulation and mucosal immunology. Then, he pursued his professional career at different part of the world including International Vaccine Institute, Korea; USDA, USA; NIH, USA and Gothernburg University, Sweden. He has published more than 150 papers in reputed journals and serves as editor of many societies including World Journal of Immunology, Frontiers in Molecular Innate Immunity, Journal of Biomaterials and Tissue Engineering. Currently, he is a president of Korean Dendritic Cell Academic Society. His interest has focused on relationship between mucosal immune respnses regarding infectious diseases and vaccine/adjuvant.

Abstract:

Alveolar macrophages treated with bioparticles, mediated through MyD88-dependent manner, are indispensable for the protection in mice infected with respiratory syncytial virus A2 (E-BABE): Respiratory syncytial virus (RSV) causes a common respiratory disease. But we have no effective ways to prevent RSV infection until now. Indeed, poor innate defense mechanisms at the initial stage of the infection brought about the serious consequences in RSV infection. One of the primary innate immune cells in the lung is alveolar macrophages (AM), which play a pivotal role to maintain homeostasis at rest and induce effective defense mechanism against infectious disease. However, a precise function of AM in RSV infected mice remains unclear. We here report that bioparticles derived from Bacillus subtilis could induce the activation of AM that played a critical function in protection against RSV infection. These bioparticels induced innate immune responses, increasing number of AM coincident with enhancing GM-CSF and IFN-γ, known as differentiation factors for classically activated macrophages (M1-macrophages). Selective depletion of AM in wild-type mice or MyD88 knock mice failed to induce IL-12p40 and impaired the clearance of dead cells associated with severe morbidity during RSV infection. Taken together, our results suggest a definitive role of AM induced by bioparticels derived Bacillus subtilis in protection from RSV infection. Biography Professor Cheol-Heui YUN completed his Ph. D. at the University of Saskatchewan, Canada in the area of immune modulation and mucosal immunology. Then, he pursued his professional career at different part of the world including International Vaccine Institute, Korea; USDA, USA; NIH, USA and Gothernburg University, Sweden. He has published more than 150 papers in reputed journals and serves as editor of many societies including World Journal of Immunology, Frontiers in Molecular Innate Immunity, Journal of Biomaterials and Tissue Engineering. Currently, he is a president of Korean Dendritic Cell Academic Society. His interest has focused on relationship between mucosal immune respnses regarding infectious diseases and vaccine/adjuvant.

Biography:

Professor Oziniel Ruzvidzo completed his doctoral degree in Plant Biotechnology in 2009 at the University of the Western Cape, South Africa. He also undertook some postdoctoral studies in the same subject area in 2010 at the University of Cape Town in South Africa. Currently, he is the Head of Department and Principal Investigator of Plant Biotechnology in the Department of Biological Sciences at the North-West University, Mafikeng Campus, South Africa, where he has already extensively published high impact factor papers in this subject area of his research specialization. Professor Ruzvidzo is an active member of several university committees including the senate as well as an editorial member of various academic and research boards locally, regionally and internationally.

Abstract:

Adenylate cyclases (ACs) are enzymes capable of converting the cellular molecule adenosine 5′-triphosphate (ATP) to the second messenger cyclic 3′,5′-adenosine monophosphate (cAMP) (Robison et al., 1968). Apparently, while in animals and other lower eukaryotes, ACs and their cAMP have firmly been established as important signaling molecules with critical roles in cellular processes like signal transduction and stress response (Gerisch et al., 1975), in higher plants however, only 4 ACs have so far been practically and experimentally confirmed. These are the Zea mays pollen protein responsible for the polarized pollen growth (Moutinho et al., 2001), the Arabidopsis thaliana pentatricopeptide repeat protein responsible for pathogen responses and gene expressions (Ruzvidzo et al., 2013), the Nicotiana benthamiana adenylyl cyclase protein responsible for the tabtoxinine-β-lactam-induced cell deaths during wildfire diseases (Ito et al., 2014), and the Hippeastrum hybridum adenylyl cyclase protein involved in stress signalling (Swiezawska et al., 2014). With continued work in this specific field domain, a recent study has further propossed an array of at least 14 other AC-encoding gene candidates in the Arabidopsis genome, and based on the functionally assigned amino acids in the catalytic center of annotated and/or experimentally tested nucleotide cyclases in lower and higher eukaryotes (Gehring, 2010). Our work therefore, is presently involved in the recombinant expression and functional characterization of these proposed AC genes to try and elucidate their possible physiological roles in stress response and disease resistance mechanisms. To date, 4 of these candidate genes have already been fully characterized, with some intriguing outcomes, while more work is still underway with the rest of the other genes.