Abstract
Abstract In collagen-induced arthritis (CIA) of mouse, self-reactive T cells recognize a peptide antigen from type II collagen (CII). CII is of particular interest, as an autoimmune response to this protein leads to CIA in mice, rats, and primates. Activation of T cells is believed to be an important pathogenic factor in autoimmune disease. So, T cells have become a focal point of study for the development of novel therapeutic approaches to the treatment of autoimmune disease. In this study, we evaluated the efficacy and mechanism of recombinant MHC II molecules in regulation of the antigen-specific T cell clones by using mouse I-Aq, combined with an auto-antigen peptide from type II collagen (CII260-274) in CIA model. It was found that recombinant I-Aq/CII260-274 molecules not only activate CII-specific T cell clone but also inhibit the same clone in vitro according to the condition of stimulation. Furthermore, development of CIA in mice was successfully prevented by the in vivo injection of a recombinant soluble I-Aq/CII260-274. Thus, recombinant soluble MHC II molecules, complex with the immuno-dominant self peptide, offer a new possibility for the treatment of chronically active autoimmune inflammation such as rheumatoid arthritis.
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