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Rheumatoid arthritis (RA) is a chronic inflammatory disease with a variable disease outcome, and is characterized with synovitis, erosive changes of the joints, pain and functional deficit. Etiology is unknown. In the pathogenesis of rheumatoid arthritis the key role have proinflammatory cytokines, particularly, tumour necrosis factor (TNFalpha). The prognosis of RA patients has improved significantly during recent years, after the introduction of TNFalpha-based therapy. Despite the wide use of these biologics, their precise mechanisms of action in RA remain unclear. In the K/BxN mice, glucose-6-phosphate isomerase (GPI) is an autoantigen recognized by T and B cells. Recombinant GPI immunization to DBA/1 mice also induced acute severe arthritis. This arthritis was clearly controlled by anti-TNFalpha Abs, suggesting similar etiology to RA. In this study, to understand the mechanisms of arthritis that was regulated by TNFalpha, we focused on TNFalpha-induced adipose-related protein (TIARP) in the generation of GPI-induced arthritis.

The role of TNF.ALPHA.-induced adipose-related protein (TIARP) in TNF.ALPHA. dependent arthritic model-GPI-induced arthritis