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r a c t ─A New Paradigm for Pathogenesis of Rheumatoid ArthritisJae-Hong Park*, M.D., Ph.D., Hyung-Bae Park†,M.S., Sungsoo Jung*†, M.D., Ph.D.The Hospital for Rheumatic diseases*, Institute of Rheumatism†,Hanyang University, Seoul, KoreaAn important role for T cells, B cells, and other leukocytes such as dendriticcells, macrophages, and neutrophils in the pathogenesis of rheumatoid arthritis(RA), has been argued. There is no consensus by reasons of the heterogeneityof RA and a dearth of small animal models of RA. We review a new paradigmfor pathogenesis of RA in the light of recent results from K/BxN (KRNC57BL/6 TCR transgenic x NOD) mice in which a spontaneous inflammatoryarthritis, similar to human RA is developed. Disease in these animals is focusedspecifically on the joint but stems from autoreactivity to an ubiquitouslyexpressed antigen, glucose-6-phosphate isomerase (GPI). Anti-GPI immunoglob-ulin-induced arthritis critically depends on innate immune system players suchas Fc receptors and the alternative pathway of complement network. New evi-dence revives the old idea that B cells are the principal effectors in RA. Inter-ventions targeting the GPI-anti-GPI immune complex would constitute a newtherapeutic strategy for RA.