Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 2nd International Conference on Clinical & Cellular Immunology Hampton Inn Tropicana, Las Vegas, USA.

Day 1 :

Keynote Forum

Charles J. Malemud

Case Western Reserve University, USA

Keynote: Role of the Interleukin-6 Receptor in Matrix Metalloproteinase Gene Expression in Human Chondrocytes

Time : 10:00-10:25

OMICS International Immunology Summit-2013 International Conference Keynote Speaker Charles J. Malemud photo

Charles J. Malemud received the Ph.D. from George Washington University in 1973 and completed postdoctoralrnstudies at the State University of New York at Stony Brook in 1977. Since 1977, Dr. Malemud has been a memberrnof the faculty at Case Western Reserve University School of Medicine where he is presently Professor of Medicinern& Anatomy in the Division of Rheumatic Diseases and Senior Investigator in the Arthritis Research Laboratory.rnHe has published more than 190 papers, chapters and reviews primarily in the field of chondrocyte biology.rnProfessor Malemud is on the editorial board of several rheumatology, immunology and musculoskeletal journalsrnand is Editor-in-Chief of the Journal of Clinical and Cellular Immunology.


T/C28a2 and C28/I2 are immortalized juvenile human chondrocytes that transcribe the cartilage-specificrntranscription factor, SOX9. We employed T/C28a and C28/I2 to examine the extent to which recombinant humanrn tumor necrosis factor- (rhTNF-), rhIL-6, oncostatin M (rhOSM) and adiponectin (rhAPN)-induced activation ofrnthe SAPK/MAPK and JAK/STAT signaling pathways and whether these signaling pathways influenced inductionrnof apoptosis. STAT1, STAT3 and STAT5 were constitutively phosphorylated in T/C28a2. Constitutivernphosphorylation of these STAT proteins was JAK-dependent since the JAK inhibitors, ruxolitinib and WHIP-131, rnreduced STAT phosphorylation. By contrast, in C28/I2, STAT3 was the most abundant STAT protein andrnphosphorylation of STAT3 (i.e. P-STAT3) was induced by rhIL-6, rhOSM and rhAPN. Of note, treatment ofrnC28/I2 suspension cultures with rhIL-6, soluble IL-6 receptor (sIL-6r), IgG4, tocilizumab, an IgG1 monoclonalrnantibody which neutralizes IL-6/IL-6 receptor binding, or the combination of rhIL-6 and tocilizumab increased USTAT1Arnand U-STAT1B. rhOSM and rhAPN, but not rhIL-6, increased P-ERK by 57% and 35%, respectivelyrnand U0126, an upstream inhibitor of ERK1/2 activation through inhibition of MEK1/2, reduced P-ERK to controlrnlevels. None of the IL-6-type cytokines increased P-JNK or P-p38. rhTNF- induced apoptosis measured by thernTUNEL assay in C28/I2 with the frequency of TUNEL-positive C28/I2 chondrocytes further increased by therncombination of rhTNF- and U0126. Apoptosis was also increased by rhIL-6 but not by rhIL-6 and U0126, nor byrnrhOSM. (Support provided by Genentech/Roche Group and 5P30EY11373 from the National Eye Institute)

Break: Coffee Break 10:25-10:40 @ Foyer

Keynote Forum

Michael G. Hanna

Vaccinogen, Inc., USA

Keynote: The impact of genomic sequencing data in cancer immunotherapy

Time : 10:40-11:05

OMICS International Immunology Summit-2013 International Conference Keynote Speaker Michael G. Hanna photo

He is the founder of Vaccinogen and the discoverer and developer of OncoVAX® an autologous vaccine designedrnto provoke a specific immune response against colon cancer cells. His previous accomplishments includernChairman (Emeritus) and Chief Scientific Officer of Intracel Resources, Chief Operating Officer of OrganonrnTeknika/Biotechnology Research Institute and Sr. Vice President of Organon Teknika Corporation. Prior to thatrn(1975-1982) Dr. Hanna was Director of the National Cancer Institute, Frederick Cancer Research Center.rnOncoVAX® is an autologous vaccine designed to provoke a specific immune response against colon cancer cells.rnThe product is comprised of irradiated tumor cells obtained from the patient after surgery and it is administeredrnalong with the BCG vaccine. Vaccinogen believes OncoVAX® is the first product to show a significant reductionrnin recurrence of disease in Stage II colon cancer patients in a major, long-term clinical trial. Except for surgery,rnthere is no medically accepted treatment for Stage II colon cancer. Trials using adjuvant chemotherapy have notrndemonstrated any patient benefit to date.rnHe led the team that achieved FDA regulatory approval of TICE BCG for treatment of carcinoma in situ (CIS)rnbladder cancer. Worldwide registration was achieved in 1991 and it is standard of care for prophylaxis ofrnrecurrence of superficial bladder cancer and therapy of CIS.rnHe received a doctoral degree in experimental pathology and immunology from the University of Tennessee. Hernhas over 225 publications to his credit, has 11 patents in immunotherapy and has been the recipient of numerousrnhonors, and served on many editorial boards


At the cellular level it is clear that cancer is a genetic disease arising as a clone that expands and grows in anrnunregulated manner. While it has always been presumed that neoplasia is a consequence of somatic cell mutations,rnonly in the last few years has the magnitude and diversity of these mutations been elucidated by modern DNArnsequencing technology. Immunotherapy is the premier biological approach to targeted therapy. Target therapiesrnrequire targets. In this case the targets are tumor specific or associated antigens, the proteins expressed from thesernsomatic cell mutations. While the immunotherapeutic approach to eliminating cancer was launched with thernassumption that cancer cells were homogeneous, the recent genomic understanding of tumor cells indicates thatrnthere is both inter- and intra-tumoral heterogeneity. This presentation will discuss the consequences of this newrnknowledge of tumor cell biology to the immunotherapeutic approach to treating cancer.

Keynote Forum

Timothy B. Niewold

Mayo Clinic, USA

Keynote: Type i interferon in human autoimmune disease

Time : 11:05-11:30

OMICS International Immunology Summit-2013 International Conference Keynote Speaker Timothy B. Niewold photo

Niewold is a human geneticist and translational researcher, bridging the traditional gap between the basic andrnclinical sciences. His work focuses on identifying and understanding the pathogenic factors in human autoimmunerndisease, and the ways in which underlying genetic factors impact immune responses. Dr. Niewold is recognizedrnfor important contributions to our understanding of how genes influence pathogenic cytokine patterns that give risernto human disease. He has published more than 80 papers in the fields of Immunology and Genetics, and is arnmember of numerous editorial boards and advisory committees, including the Scientific Advisory Committee ofrnthe American College of Rheumatology Research Foundation, and the Editorial Board of Arthritis andrnRheumatism, the official journal of the American College of Rheumatology. He also directs the Federation ofrn Clinical Immunology Societies Centers of Excellence, a group of 68 centers at major academic institutions in thernUnited States and around the world that are focused on human immunology studies.


The type I interferon system plays a critical role in host defense in health, and a growing body of literaturernsuggests that type I interferon is a critical mediator of human autoimmune disease. Type I interferons function asrna bridge between the innate and adaptive immune systems, and as such plays an important role in settingrnthresholds for response against self antigens. We have studied type I interferon responses in a number ofrnautoimmune diseases, including systemic lupus erythematosus, dermatomyositis, multiple sclerosis, neuromyelitisrnoptica, and others. In this plenary session, I will summarize our findings and the pathogenic implications of therntype I interferon system in human autoimmune disease pathogenesis. Major topics will include how geneticrnvariations impact type I interferon responses in humans, and how activation of this pathway corresponds withrnparticular disease features, providing a window into human disease pathogenesis.

Keynote Forum

Jianfei Yang

Tempero Pharmaceuticals, a GSK Company, USA

Keynote: Small molecule inhibitors targeting the Th17 cell transcription factor RORgt for the treatment of autoimmune diseases

Time : 11:30-11:55

OMICS International Immunology Summit-2013 International Conference Keynote Speaker Jianfei Yang photo

Jianfei Yang is a Principal Scientist and a Project Leader of a Th17 cell-related project at TemperornPharmaceuticals, a GSK company, in Cambridge, MA, USA. He received a PhD in Pathology from NiigatarnUniversity in Japan in 1997. He then obtained postdoctoral training in Dr. Ken Murphy’s lab at HHMI andrnWashington University. In the past 16 year, he has been studying the role of CD4+ T helper cells in immunity andrndiseases. He has more than 10 years of experience in autoimmune disease research and pharmaceutical drugrndevelopment. He has published numerous papers and patents.


CD4+Th17 cells, which are characterized by the expression of IL-17A, IL-17F, IL-22, IL-23R and CCR6, havernbeen shown to play a critical role in a variety of autoimmune diseases including rheumatoid arthritis, multiplernsclerosis, psoriasis, inflammatory bowel disease, and asthma. IL-23 is critical for the differentiation of Th17 cellsrnin vivo. Genome-wide association studies have demonstrated thatIl23r polymorphisms are associated with severalrn autoimmune diseases. Further, monoclonal antibodies against IL-12/IL-23p40 or IL-23p19 have shown spectacularrnefficacy in psoriasis patients. However, these antibodies target only a single cytokine and have limited efficacy inrnother autoimmune diseases. Thus, targeting Th17 lineage should result in better efficacy. The nuclear receptorrnRORgt has been shown to be the master transcription factor for the differentiation of Th17 cells as well as thernexpression of Th17 signature genes. We and several academic labs have discovered small molecule inhibitors ofrnRORgt for the treatment of various diseases. The biology of RORgt has been extensively studied using ROR─▒trnsmall molecule inhibitors as tool compounds. The very recently advance of RORgt biology and its clinicalrnapplication will be discussed.

Keynote Forum

Sergei A. Grando

University of California, USA

Keynote: tittle

Time : 11:55-12:20

OMICS International Immunology Summit-2013 International Conference Keynote Speaker Sergei A. Grando photo

Grando is a board-certified dermatologist with more than 30 years experience. He is a leading expert andrnresearcher in eczema and other autoimmune blistering diseases. He is conducting a clinical trial for the treatmentrnof pemphigus with a non-hormonal medication. Grando has published more than 225 papers, monographs andrnbook chapters, and has been awarded numerous research grants from the National Institutes of Health and otherrnfunding agencies. He was awarded as a Doctor of the Year, 2010, International Pemphigus and PemphigoidrnFoundation and Vice Chair, a medical advisory board of the International Pemphigus and Pemphigoid Foundation.rnHis Academic Distinctions includesrn2010- present Vice Chair, Medical Advisory Board of International Pemphigus and Pemphigoid Foundationrn2005-Honorary Chair for California, NRCC Physicians' Advisory Board.rn2004- Vice Chair, Dermatology Foundation of Californiarn2002-present Honorary Member Ukrainian Association of Dermatologists, Venereologists, Cosmetologists,rnUkrainern2001-Clinical Innovator Award, Flight Attendant Medical Research Institute, USArn1995-FIRST Award, NIH, NIAMS, USA and He have 250 publications.


Current understanding of pemphigus vulgaris (PV) does not explain acantholysis in patients lacking desmogleinrnantibodies. PV IgGs enter keratinocytes (KCs) and specifically bind to mitochondrial proteins, which is associatedrnwith mitochondrial damage triggering apoptosis and acantholysis. Using a protein microarray approach, we havernpreviously demonstrated that mitochondrial proteins most commonly targeted in PV are involved in oxidativernphosphorylation, O2 respiration, production/inactivation of reactive oxygen species (ROS), and tricarboxylic acidrncycle. In this study, we sought to identify changes in the vital mitochondria functions in KCs treated with the serarnfrom PV patients and healthy donors. PV sera significantly increased proton leakage from KCs, suggesting thatrn PV IgGs increase ROS production and reduce the ability of KCs to respond to stress. Indeed, measurement ofrnintracellular ROS production by the c-H2DCFDA-AM dye labeling of cultured KCs showed a drastic increase ofrncell staining in response to treatment by PV sera, which was confirmed by FACS analysis. Exposure of KCs tornPV, but not normal, sera also caused dramatic changes in the mitochondrial membrane potential detected with thernJC-1 dye. This observation indicated that binding of PV IgGs to mitochondrial target proteins disrupts the electronrntransfer chain resulting in loss of electrochemical gradient across the inner membrane. The results of thisrnstudyhelp explain the mechanism of therapeutic action of mitochondria-protecting drugs, such as nicotinamide, rnminocycline and cyclosporine, in PV patients and suggest novel avenues for development of personalizedrntherapies based on the pharmacological correction of mitochondrial abnormalities in individual PV patients.

Break: Panel Discussion 12:20-12:30
Lunch Break 12:30-13:15 @ Carol & Patio