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10th Cytokines and Inflammation Conference

  October 20, 2011  
GTC Conferences, United States
2012-01-30 to 2012-01-31

10th Cytokines and Inflammation Conference • Jan 30-31, 2012 • San Diego, CA, USA
Register by November 29 for a 20% Discount. Or Register 2, the 3rd goes free with the coupon code rcdvb!

Day 1Day 2
Day 1 - Monday, January 30, 2012
7:00Registration & Continental Breakfast
7:55Welcome & Opening Remarks
8:00Type 1 Interferons Exacerbate Th17 Autoimmunity
 Lawrence Steinman, Professor, Neurology and Pediatrics, Stanford University
 The various forms of recombinant IFN-b are the most widely used therapeutics for relapsing remitting multiple sclerosis (RRMS). Despite their wide use, only about half of RRMS patients respond well to this treatment, and some patients have exacerbations while taking them. Despite expenditures in excess of $4 billion in annual sales, there is no rational way to decide whether or not someone will benefit from IFN-b. We published in Nature Medicine that the clinical response to IFN-b; therapy is strongly influenced by the Th1/Th17 ‘pathways’. EAE induced with pathogenic TH1 T cells is prevented when IFN-b treatment is given prior to therapy, and that clinical deficits and pathology are reversed, even when IFN-b is given after mice are paralyzed. In contrast, TH17 EAE is exacerbated clinically and inflammation in the central nervous system is increased following administration of IFN-b. We found that serum levels of IL-17F are elevated in a subset of non-responders prior to treatment, Non-responders had relapses in the two years after treatment, while responders were relapse free. A combination of low IL-17F and high IL-7 predicted responsiveness to type 1 interferon. Of interest, a rare demyelinating disease, known as neuromyelitis optica-NMO, is characterized by high levels of IL-17. NMO is exacerbated when IFN-b treatment is given. NMO may actually represent an already described version of a Th17 demyelinating disease. Type 1 interferons should not be given to individuals with Th17 autoimmune diseases.
Cytokines Regulation
8:35Anti-inflammatory Actions of Glucocorticoids: Unexpected Players and Mechanisms
 Inez Rogatsky, Ph.D., Associate Professor, Research Division, Hospital for Special Surgery and Dept of Microbiology and Immunology, Weill Medical College of Cornell University
 Dysregulated production of proinflammatory cytokines is linked to tissue damage, inflammatory diseases and autoimmunity. Inflammation is counteracted by the endogenous or clinically administered glucocorticoids (GCs) which prompt the intracellular transcription factor – the GC receptor (GR) – to suppress inflammatory gene expression, however the underlying molecular mechanisms remain obscure. Furthermore, a given inflammatory signal induces panels of genes with distinct kinetics suggesting that mechanisms of activation and, consequently, repression are likely to vary. Our earlier studies suggested that GR-mediated repression may involve a transcriptional coregulator GRIP1 of the p160 family, yet the role of GRIP1 in cytokine gene expression or in inflammation in vivo has never been examined.

We analyzed transcription complex assembly and function at several proinflammatory genes in murine primary macrophages (M
F) and found that genes fall into distinct classes depending on the rate-limiting step of the transcription cycle (activation vs. early elongation) at which they are activated. Interestingly, irrespective of the TLR pathway responsible for the induction, genes in both classes were dramatically repressed by liganded GR. To address the role of GRIP1 in GR-mediated suppression of inflammation, we generated conditional GRIP1-deficient mice. The transcriptome analysis of GRIP1-deficient MF activated with TLR ligands in the absence or presence of GCs and the effects of GRIP1 deletion in inflammatory response in vivo will be presented.
9:00Regulation of IL-15 Revealed with a Novel Reporter System
 Leo Lefrancois, Ph.D., Professor and Chair, Immunology; Director, Center for Integrative Immunology and Vaccine Research, University of Connecticut Health Center
 Interleukin-15 (IL-15) plays a multifaceted role in immune homeostasis, but the unreliability of IL-15 detection has stymied exploration of IL-15 regulation in vivo. To visualize IL-15 expression, we created a transgenic mouse expressing emerald-GFP (EmGFP) under IL-15 promoter control. EmGFP/IL-15 was prevalent in innate cells including conventional dendritic cells (cDCs), macrophages, and the granulocytic lineages such as basophils and neutrophils. However, individual DC subsets expressed varying levels of EmGFP/IL-15 depending on their phenotype and anatomical location. In the spleen, CD8+ DCs expressed significantly higher levels of EmGFP/IL-15 than the CD8subset, while plasmacytoid DCs were negative for EmGFP/IL-15 expression. However, the CD11cintMHCIIhigh migratory DCs in the peripheral lymph nodes (LNs) expressed the highest levels of EmGFP/IL-15 of any DC subset during steady state. Analysis of hematopoietic progenitors revealed high EmGFP/IL-15 expression in LSK (Lin-Sca-1+c-kit+) cells that progressively waned as cells matured towards a DC fate. EmGFP/IL-15-expressing pre-cDCs could generate both EmGFP/IL-15int CD8+ and EmGFP/IL-15low CD8mature DCs, revealing regulatory control of IL-15 expression throughout DC development. Interestingly, EmGFP/IL-15 expression was also downregulated as early thymic progenitors progressed through the double negative stage of T cell development in the thymus yielding EmGFP/IL-15neg ab T cells and EmGFP/IL-15low gd T cells in the periphery. A small subset of gd T cells in the peripheral, but not mesenteric, LNs expressed high levels of EmGFP/IL-15 and largely corresponded to the naturally occurring CD44highCD62LlowCD27lowCCR6high IL-17-producinggd T cells that exist in uninfected mice. Lastly, the induction of inflammation through virus infection resulted in EmGFP/IL-15 upregulation that was differentially controlled in cDC subsets by type I IFN. These findings provide evidence of previously unappreciated differences in IL-15 production between individual DC subsets during development, homeostasis and following viral infection, and identify gd T cells as a novel source of IL-15 in secondary lymphoid organs.
9:25A Chromatin-based High-throughput Screen for Selective Regulators of Pro-inflammatory Cytokine Genes
 Stephen T. Smale, Ph.D., Professor and Vice Chair, Microbiology, Immunology and Molecular Genetics; Director, Basic/Translational Research, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA
 Inflammation can be beneficial for a normal immune response to microbial pathogens. However, prolonged inflammation can promote tissue damage and has been closely linked to a diverse range of diseases, including several inflammatory autoimmune diseases, cancer, and atherosclerosis. Although a number of anti-inflammatory drugs are available, new strategies are needed for the development of selective inhibitors of pro-inflammatory genes and proteins. Our laboratory has had a long-standing interest in the contributions of chromatin structure to pro-inflammatory cytokine gene transcription. We have carried out in depth studies of chromatin structure and nucleosome remodeling at the IL12B gene, which encodes the p40 subunit of IL-12 and IL-23, and we have classified pro-inflammatory genes on the basis of chromatin and promoter properties. Most recently, we have taken advantage of the important role of chromatin in selective gene transcription to develop a high-throughput screening strategy for the identification of selective modulators of inflammatory cytokine genes, using the IL12B gene as an initial model. This screening strategy allowed us to identify compounds that selectively inhibit transcription of the IL12B gene or limited subsets of inducible genes, while excluding compounds that target broad regulators of inducible gene transcription, such as NF-kB. The targets and mechanisms of action of the selective inhibitors are currently being pursued.
9:50Networking & Refreshment Break
10:20TSLP and Allergic Inflammatory Diseases
 Rene De Waal Malefyt, Department of Immunology, Merck
10:45Marco Londei, Translational Science GNF, Novartis - Tentative
Cytokines in Health and Disease
11:10Linda C. Burkly, Ph.D., Distinguished Investigator, Immunobiology, Biogen Idec
11:35Negative Regulation of Cytokine Signaling Defines An Unexpected Dendritic Cell Checkpoint: Impact on Autoimmunity
 Pamela S. Ohashi, FRSC, Ph.D., Co-Director, Senior Scientist and Professor, Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute/University Health Network and University of Toronto
 My lab has been interested in understanding the important signals that occur during dendritic cell: T cell interactions that lead to the breakdown of tolerance and result in autoimmunity. We have unexpectedly identified a profound role for TNF? in breaking tolerance, and perhaps an equally unexpected finding showing that IL-12 is not essential for this process.

In order to gain further insights into DC: T cell interactions that are critical for breaking tolerance, we have generated a new way to induce diabetes using our RIP-GP transgenic model. For many years we have worked on the RIP-GP mouse, where the lymphocytic choriomeningitis virus glycoprotein (LCMV-GP) is expressed on the ?-islet cells of the pancreas. Our previous studies have shown that virus infection in RIP-GP mice, or P14/RIP-GP double transgenic mice treated with peptide and DC maturation signals (anti-CD40, TLR, HSP-70) leads to the induction of tissue specific immunity and diabetes. We have recently developed a model showing that TLR matured bone marrow derived DCs pulsed with GP peptides can induce diabetes in RIP-GP single transgenic mice within 10 days. This allows us to evaluate different properties of DCs using bone marrow from gene deficient mice. It also allows us to investigate the consequences of maturing DCs with different TLR stimuli and the consequences on the adaptive immune system in vivo. 

I will present data on our recent studies identifying a molecule that is responsible for maintaining DCs in a resting state. In its absence, autoimmunity can be induced without the need for TLR maturation signals, via a TNF? dependent mechanism. We have also shown that DCs matured with different TLR stimuli can induce diabetes, but interestingly impose different cytokine requirements to promote tissue specific responses in vivo.
1:30Carl Ware, Ph.D., Professor, Laboratory of Molecular Immunology; Director, Infectious and Inflammatory Disease Center,Sanford-Burnham Medical Research Institute
1:55Xiaoxia Li, Ph.D., Professor, Cleveland Clinic
2:20  Harold M. Hoffman, M.D., Associate Professor, Pediatrics and Medicine, University of California, San Diego
2:45Revisiting Human TYK2 Deficiency
 Stephanie Boisson-Dupuis, Ph.D., Senior Research Associate, The Rockefeller University
3:10IL-1 Blockade in Acute Myocardial Infarction and Heart Failure
 Antonio Abbate, M.D., Ph.D., Assistant Professor, Medicine, VCU Pauley Heart Center, Virginia Commonwealth University
3:35Networking & Refreshment Break
Translational Medicine
4:05Translational Medicine in Immunology through Four Success Stories
 Francisco Leon, M.D., Ph.D., Vice President, Immunology Translational Medicine, Janssen, a division of Johnson & Johnson
 Translational research can be defined as the bi-directional process of applying clinical knowledge to basic research and scientific knowledge to clinical development. The benefits of translational research are shorter clinical development timelines and reduced risk by enabling earlier and more robust science-based decision making. 

The Translational Medicine session will review 4 success stories as examples of translational research put into practice. The talks will cover autoimmunity, allergy and transplantation and will illustrate the journey of several breakthrough medicines from the lab to the patients who need them.
4:15Belatacept: Fine Tuning Co-stimulation Blockade – From Bench to Bedside
 Robert Townsend, Director, Clinical Biomarkers, BMS
4:40Targeting the Type 1 Interferon Pathway for the Treatment of Lupus
 Roland Kolbeck, Director, Respiratory, Inflammation and Autoimmunity, MedImmune
5:05IL-13 in Inflammatory and Allergic Diseases
 Peter J. Mannon, M.D., M.P.H., Professor, Medicine, Division of Gastroenterology and Hepatology, The University of Alabama at Birmingham
 Interleukin-13 is emerging as an important cytokine in gastrointestinal disease beyond its role in allergic inflammation, intestinal helminth infection and tissue fibrosis. Animal models and clinical studies in humans show IL-13 playing a unique pathologic role in ulcerative colitis and eosinophilic esophagitis. The importance of these data is reflected in several new clinical trials studying the effects of IL-13-targeted agents in these gut diseases. Furthermore, other recent data describing IL-13 production by “innate helper cells” under the influence of epithelial factors and IL-13 regulation of Th17 cells points to relevance for gut mucosal immunology.

This talk will highlight:
1. Relevance of IL-13 to intestinal mucosal homeostasis and pathology (specifically ulcerative colitis) supported by data from preclinical models, ex-vivo human tissue studies, and immune monitoring during clinical trials
2. Results of preclinical/clinical trials using anti-IL-13 strategies in inflammatory disease, including ulcerative colitis and asthma, with a timeline for results of trials underway 
3. Pharmacologic profiles/mechanism of action of available anti-IL-13 agents
4. Assessment of challenges and opportunities for IL-13 in ulcerative colitis, eosinophilic esophagitis, fibrosing IBD, and asthma
 5:30Kim Campbell, Ph.D., Director, Immunology Product Support, Janssen, a division of Johnson & Johnson
Panel Discussion: Translational Medicine
5:55Panel Discussion
6:15Networking Reception and Poster Session

Day 1Day 2
Day 2 - Tuesday, January 31, 2012
Inflammation and Cancer
8:00Chemokine and Toll-like Receptors (TLR) Cross-talk With Neuropeptide Algesic Receptors (TRPV1) Enhances Painful Inflammatory Reactions
 Joost J. Oppenheim, M.D., Chief, Laboratory of Molecular Immunoregulation, NIH, NCI
 Chemokine receptor cross-talk suppresses analgesic opioid receptors, but stimulates algesic TRPV1 receptors, thus promoting pain. Painful Herpes Zoster infection due to herpes virus (VZV) induces mediators that enhance the expression of TLR3, 7 and 9 by peripheral neurons present in dorsal root ganglia (DRG). Stimulation of these TLR, in turn induces chemokines and transactivates TRPV1 resulting in enhanced calcium flux by capsaicin stimulated TRPV1. Thus VZV by inducing TRPV1 can cause severe neuralgia. Furthermore, in a mouse tumor model treatment with suppressive oligonucleotides that inhibit TLR9 suppressed sensitivity to pain due to heat, which is mediated by TRPV1. Consequently stimulation of DRG neurons by TLR ligands can directly and indirectly cause nerve pain.
8:35Inflammasome-dependent and Independent Pathways of Sterile Inflammation
 Kenneth L. Rock, M.D., Professor and Chairman, Pathology, University of Massachusetts Medical School
 The inflammatory response plays a key role in host defense. It mobilizes innate immune defenses that attempt to neutralize infections and injurious agents and promote tissue repair. This response comes at a cost to the host because it creates symptoms, such as pain, and causes collateral damage in tissues. However, this is a small price to pay to contain an infection that could become life threatening. Iin contrast, inflammation can also be elicited by sterile stimuli and in these situations the inflammation may do more harm than good and actually cause disease. A potpourri of stimuli can cause sterile diseases, a subset of which are sterile irritant particles (e.g. urate crystals in gout, silicates in silicosis, dead cells, and cholesterol crystals in atherosclerosis). Although structurally diverse these particles stimulate inflammation through common pathways that lead to the production of bioactive IL-1. Some of this IL-1 is produced when the particulate stimuli lead to the activation of inflammasomes to process pro-IL-1b into mature IL-1. In addition, there are inflammasome-independent pathways that lead to the production of bioactive IL-1. Our current understanding of these mechanisms and their contribution to disease will be discussed.
9:00Chen Dong, Ph.D., Professor, Department of Immunology, Director, Center for Inflammation and Cancer, MD Anderson
9:25[Oral Presentations from Exemplary Submitted Abstracts]
 To be considered for an oral presentation, please submit an abstract here by December 30, 2011.
10:00Networking & Refreshment Break
Novel Technological Developments in Cytokines
10:30Mechanisms Involved in Strong Activity of Cytokine/mAb Complexes
 Charles D. Surh, Ph.D., Professor, Immunology & Microbial Science, IMM26, The Scripps Research Institute
10:55J. Fernando Bazan, Chief Scientific Officer, NeuroScience - Tentative
11:20Zehra Kaymakcalan, Ph.D., Senior Principal Scientist, Biologics, Abbott
11:45Jennifer Towne, Principal Scientist, Amgen - Tentative
Therapeutic Applications of Cytokines and Chemokines
1:15Phillip K. Weck, Ph.D., Vice President and Compound Development Team Leader, Centocor R&D
1:50PEGylated Interferon Beta-1a: Meeting an Unmet Medical Need in the Treatment of Relapsing Multiple Sclerosis
 Darren P. Baker, Ph.D., Associate Director, Protein Biochemistry, Biogen Idec
 Relapsing multiple sclerosis (RMS) is a chronic autoimmune disease of the central nervous system for which a number of disease modifying therapies are available. Although such drugs are efficacious, significant numbers of diagnosed individuals remain untreated, including those with relatively mild disease who choose not to initiate therapy, those wary of parenteral administration (i.e. injections), and those who stop therapy due to intolerance or a perceived lack of efficacy. Since these drugs may require frequent administration that may affect a patient’s decision to initiate and stay on therapy, there is a need for a treatment that is safe and efficacious but that requires a more convenient dosing regimen. For the interferon beta products approved to treat multiple sclerosis, the frequency of administration ranges from once weekly (Avonex®, BiogenIdec), to 3 times per week (Rebif®, Merck-Serono), and every other day (Betaseron/Betaferon®, Bayer; Extavia®, Novartis). With the aim of improving the pharmacokinetic properties of interferon beta, and potentially its pharmacodynamic properties, and also to reduce the frequency of administration thereby reducing the frequency of side effects associated with interferon beta treatment, a PEGylated form of interferon beta-1a is being developed. The presentation will summarize the development of this molecule from Discovery Research through to Phase 3 clinical testing.
2:15Raymond Donnelly, Ph.D., Senior Investigator, Division of Therapeutic Proteins, FDA Center for Drug Evaluation & Research
2:40Oncogenic IL-7R Gain-of-function Mutations in Childhood T-ALL
 Scott K. Durum, Ph.D., Chief, Section of Cytokines and Immunity, NIH, NCI
 T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy resulting from leukemic transformation of T-cell progenitors in the thymus. It accounts for approximately 15% of ALL cases in childhood and 20-25% in adults and is a leading cause of death in children. IL-7 and its receptor (IL-7R) play a critical role in normal T-cell development and homeostasis. Mutations in IL-7R were indentified in 9% of pediatric T-ALL patients. These mutations usually involved insertions of three amino acids including cysteine and proline in the extracellular juxtamembrane region. WT or mutant forms of the human IL-7R (hIL-7R) from patients were retrovirally transfected into an IL-7-dependent murine thymic cell line D1. Mutant hIL-7Rs induced ligand-independent activation of the Jak-Stat and PI3K pathways, cell survival and proliferation. Notably, mutant hIL-7R-expressing D1 cells induced subcutaneous tumors in Rag1-/- mice, with substantial infiltration into various organs that are normally affected in advanced stages of T-ALL, such as bone marrow, liver, lymph nodes and spleen. Further functional assays revealed that mutant hIL-7Rs constitutive signaling required homodimerization via cysteines in the inserted sequences and downstream Jak1 activation, and was IL-7, gc and Jak3-independent. Our findings indicate that hIL-7R mutational activation drives T-ALL leukemogenesis and implicate IL-7R and Jak1 as therapeutic targets in T-ALL.
3:05Inhibition of Binding of Acetylated Histones by Bromodomain-containing Proteins Differentially Modulates Cytokine Production from CD4T Cells and Limits the Pathogenicity of Autoreactive T cells
 Hozefa Bandukwala, La Jolla Institute of Allergy and Immunology
 A diverse group of bromodomain-containing proteins bind acetylated lysine residues on histone tails and are involved in the recruitment of additional factors that enable transcription as well as mediate post-translational modification of histones. A compound, that inhibits binding of an acetylated histone peptide to BRD4 and other proteins of the BET (bromodomain and extra-terminal domain) family, was previously shown suppress the production of pro-inflammatory proteins by macrophages and block acute inflammation in mice. We have investigated the effect of this compound on T cell function. We show that treatment of naïve CD4+ T cells with this compound during early differentiation modulates subsequent cytokine production, and inhibits the ability of Th1-skewed cells to induce subsequent autoimmune pathogenesis in a model of experimental autoimmune encephalomyelitis (EAE) in vivo. The suppressive effects of the compound on T-cell mediated inflammation were not due to inhibition of expression of the pro-inflammatory cytokines, IFN-g; or IL-17, but correlated with ability to suppress GM-CSF production from CNS-infiltrating T cells, resulting in decreased recruitment of macrophages and granulocytes. These effects were distinct from those of the fumarate ester, dimethyl dumarate (DMF), a candidate drug for treatment of multiple sclerosis (MS). Our data suggest that inhibitors of BET-family proteins and DMF could have complementary roles in the treatment of MS, and provides a strong rationale for the use of BET inhibitors in the treatment of autoimmune diseases, based on their dual ability to suppress granulocyte and macrophage recruitment by T cells as well as production of pro-inflammatory proteins by macrophages. 

Talk highlights.
1. Evaluation of Bromodomain containing proteins as novel target for limiting inflammation
2. Selective dysregulation of chemokine and cytokine expression by targeting pTEFB
3. Novel genes that influence T cell mediated inflammation. 
4. Combinatorial therapies for limiting inflammation in EAE
5. Selective Inhibition of RORgt function
3:30Chemokine Receptors Inhibitors as Human Therapeutics: Closing the Gap Between Preclinical Science and Positive Data from Clinical Trials in Rheumatoid Arthritis, Inflammatory Bowel Disease, and Diabetes
 Thomas J. Schall, Ph.D., President and Chief Executive Officer, ChemoCentryx
 Chemokines and their receptors are central to the inflammatory process and are very attractive therapeutic targets. Nevertheless, the history of drug development targeting chemokine receptors has presented many challenges and, until very recently, more failures than success. Work in my laboratories over the last 2 decades has ranged from discovery of new chemokine receptors, development of novel screening technologies (such as the RAM Assay = Reverse Activation of Migration) for drug discovery; developing significantly revised predictions from pre-clinical models of the required in vivo drug coverage levels for chemokine receptor inhibitors that will be required for therapeutic effect, and finally, completion of successful clinical trials of small molecule antagonists different chemokine receptors. These trials include inhibitors for CCR1 in rheumatoid arthritis, CCR2 in metabolic disease, and CCR9 in Crohn’s disease (the latter of which is now in Phase 3 pivotal trials). I will present new data from the lab and from clinical trials (from both ‘negative’ and successful clinical studies for chemokine receptor inhibitors) which reveal how refinements in preclinical science, including new screening technologies and more accurate assessments of pharmacokinetic / pharmacodynamics (PK/PD) models, can be can be combined with emerging data from humans in order to bring forward successful new medicines that target chemokine receptors.
4:00Conference Concludes
Organized by: GTC Conferences
Invited Speakers:
Lawrence Steinman
Professor, Neurology and Pediatrics
Stanford University
Joost J. Oppenheim, M.D.
Chief, Laboratory of Molecular Immunoregulation
Antonio Abbate, M.D., Ph.D.
Assistant Professor, Medicine, VCU Pauley Heart Center
Virginia Commonwealth University
Darren P. Baker, Ph.D.
Associate Director, Protein Biochemistry
Biogen Idec
Hozefa Bandukwala
La Jolla Institute of Allergy and Immunology
J. Fernando Bazan - tentative
Chief Scientific Officer
Stephanie Boisson-Dupuis, Ph.D.
Senior Research Associate
The Rockefeller University
Linda C. Burkly, Ph.D. 
Distinguished Investigator, Immunobiology
Biogen Idec
Kim Campbell, Ph.D.
Director, Immunology Product Support 
Janssen, a division of Johnson & Johnson
Raymond Donnelly, Ph.D.
Senior Investigator, Division of Therapeutic Proteins
FDA Center for Drug Evaluation & Research
Chen Dong, Ph.D.
Professor, Department of Immunology, Director, Center for Inflammation and Cancer
MD Anderson
Scott K. Durum, Ph.D. 
Chief, Section of Cytokines and Immunity
Harold M. Hoffman, M.D.
Associate Professor, Pediatrics and Medicine
University of California, San Diego
Zehra Kaymakcalan, Ph.D.
Senior Principal Scientist, Biologics 
Roland Kolbeck
Director, Respiratory, Inflammation and Autoimmunity
Leo Lefrancois, Ph.D.
Professor and Chair, Immunology; Director, Center for Integrative Immunology and Vaccine Research
University of Connecticut Health Center
Francisco Leon, M.D. Ph.D. 
Vice President, Translational Medicine, Immunology
Janssen, a division of Johnson & Johnson
Xiaoxia Li, Ph.D.
Cleveland Clinic
Rene De Waal Malefyt
Department of Immunology
Peter J. Mannon, M.D., M.P.H.
Professor, Medicine, Division of Gastroenterology and Hepatology
The University of Alabama at Birmingham
Pamela S. Ohashi, FRSC., Ph.D.
Co-Director, Senior Scientist and Professor
Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute
University Health Network and University of Toronto
Kenneth L. Rock, M.D.
Professor and Chairman, Pathology
University of Massachusetts Medical School
Inez Rogatsky, Ph.D.
Associate Professor, Research Division, Hospital for Special Surgery and Dept of Microbiology and Immunology
Weill Medical College of Cornell University
Thomas J. Schall, Ph.D.
President and Chief Executive Officer
Stephen Smale, Ph.D.
Professor, and Vice Chair, Microbiology, Immunology & Molecular Genetics
Co-Director, Medical Scientist Training Program; Director, JCCC Gene Regulation Program Area
Charles D. Surh, Ph.D.
Professor, Immunology & Microbial Science, IMM26
The Scripps Research Institute
Jennifer Towne, Ph.D. - tentative
Principal Scientist
Robert Townsend
Director, Clinical Biomarkers
Carl Ware, Ph.D.
Professor, Laboratory of Molecular Immunology; Director, Infectious and Inflammatory Disease Center
Sanford-Burnham Medical Research Institute
Phillip K. Weck, Ph.D.
Vice President and Compound Development Team Leader
Centocor R&D
Deadline for Abstracts: 2011-12-30
Registration: https://www.gtcbio.com/index.php?option=com_register&cn=10th%20Cytokines%20and%20Inflammation%20Conference&cid=51
E-mail: eileen.zhao@gtcbio.com
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