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RetractionAutoimmunity Free access | 10.1172/JCI17321R1
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Published November 15, 2003 - More info
CD4+ helper Th cells play a major role in the pathogenesis of rheumatoid arthritis. Th cell activation, differentiation, and immune function are regulated by costimulatory molecules. Inducible costimulator (ICOS) is a novel costimulatory receptor expressed on activated T cells. We, as well as others, recently demonstrated its importance in Th2 cytokine expression and Ab class switching by B cells. In this study, we examined the role of ICOS in rheumatoid arthritis using a collagen-induced arthritis model. We found that ICOS knockout mice on the DBA/1 background were completely resistant to collagen-induced arthritis and exhibited absence of joint tissue inflammation. These mice, when immunized with collagen, exhibited reduced anti-collagen IgM Ab’s in the initial stage and IgG2a Ab’s at the effector phase of collagen-induced arthritis. Furthermore, ICOS regulates the in vitro and in vivo expression of IL-17, a proinflammatory cytokine implicated in rheumatoid arthritis. These data indicate that ICOS is essential for collagen-induced arthritis and may suggest novel means for treating patients with rheumatoid arthritis.
Roza I. Nurieva, Piper Treuting, Julie Duong, Richard A. Flavell, Chen Dong
Original citation: J. Clin. Invest.111:701–706 (2003). doi:10.1172/JCI17321.
Citation for this retraction: J. Clin. Invest. doi:10.1172/JCI17321R1.
My colleagues and I performed collagen-induced arthritis experiments reported in the paper under the impression that this study had been approved by the Institutional Animal Care and Usage Committee (IACUC) of the University of Washington, but we were subsequently informed by this committee that such approval had not been granted. There were no scientific errors in the paper, and we stand by the validity, importance, and interest of the results. However, the paper is to be retracted according to the JCI's policy of publishing only studies that have been formally approved by an IACUC. We are sorry for any inconvenience this has caused.
Chen Dong