Rheumatoid arthritis (RA) is a systemic autoinflammatory disorder characterized by synovial hyperplasia and infiltration of inflammatory cells, as well as by the progressive destruction of cartilage and bone. Self-antigen presentation through aberrant major histocompatibility complex (MHC) class II expressing B cells produces autoantibodies, leading to development of more erosive RA. IK cytokine functions as an inhibitor of interferon γ (IFNγ)-induced MHC class II on B cells. Although its cellular and molecular mechanisms have remained unclear, IK cytokine has previously been linked to autoimmune diseases such as lupus nephritis and alopecia areata. Here, we investigated the role of IK cytokine in the pathogenesis of murine autoimmune arthritis. We generated immunodeficient arthritis mice (tIK-Tg-IL-1RaKO) by cross-breeding transgenic mice expressing truncated IK (tIK-Tg) with knockout mice lacking the IL-1 receptor antagonist (IL-1Ra-KO). In this regard, the Type II collagen (CII) immunized tIK-Tg-IL-1RaKO mice showed mild type arthritis and lower incidence than CII immunized IL-1RaKO mice. tIK-Tg-IL-1RaKO mice also showed decreased proinflammatory cytokine expression and immune cell expansion. Taken together, these results suggest that overexpression of IK cytokine may suppress the development of autoimmune arthritis by modulating inflammatory response in the case of autoimmune arthritis. Key words: IK cytokine, MHC class II, Rheumatoid arthritis
- Copyright © 2013 by The American Association of Immunologists, Inc.