3rd International Conference and Exhibition on Orthopedics & Rheumatology, July 28-30, 2014, San Francisco, USA
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Abstract
The highly pathogenic GM-CSF+IL-17+CD4 T cells and IL-23+IRF5+M1 macrophages exhibit a bidirectional interaction in autoimmunity. Death receptor 5 (.alyzed DR5 expression and apoptosis function of an anti-human DR5 antibody, TRA-8, in macrophages and T cells in humans and humanized DR5 transgenic mice in the context of collagen II-induced arthritis (CIA) and systemic autoimmune diseases. Expression of DR5 was highly correlated with that of GM-CSF in CD4 T cells and that of IL-23 and IRF5 in macrophages from synovia fluid of Rheumatoid arthritis (RA) patients. In vitro treatment with TRA-8 resulted in 94.1% and 43.4% depletion of GM-CSF+ CD4+ T cells and IL-23+ macrophages, respectively. CIA was induced inhumanized DR5 transgenic mice (Tg+).
Biography
Jun Li has received his MD from Sun Yat-sen University and his PhD (Physiology) and postdoctoral training (Immunology & Rheumatology) from University of Alabama at Birmingham (UAB). He is currently a faculty at the Division of Clinical Immunology and Rheumatology, UAB. He focuses on developing novel therapies for Rheumatoid arthritis (RA) and his major research interests include targeting M1 inflammatory macrophages in RA, regulation of macrophage plasticity by fucosylation in RA, and the bidirectional interaction between macrophages and T cells in RA. His research is funded by Arthritis Foundation. He has received multiple awards from The American Association of Immunologists (AAI). His research has also been recognized by Rheumatology Congress UK.He has served as a reviewer for Arthritis and Rheumatism, Clinical Rheumatology and other reputed journals.
camera iphone 8 plus apk Jun Li| University of Alabama at Birmingham|USA| Orthopedics 2014 | OMICS International | |
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