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Experimental & Molecular Medicine ; : 547-554, 2010.
Article in English | WPRIM | ID: wpr-200111

ABSTRACT

TGF-beta-induced tolerogenic-antigen presenting cells (Tol-APCs) could induce suppression of autoimmune diseases such as collagen-induced arthritis (CIA) and allergic asthma. In contrast, many studies have shown that NKT cells are involved in the pathogenesis of Th1-mediated autoimmune joint inflammation and Th2-mediated allergic pulmonary inflammation. In this study, we investigated the effect of CD1d-restricted NKT cells in the Tol-APCs-mediated suppression of autoimmune disease using a murine CIA model. When CIA-induced mice were treated with Tol-APCs obtained from CD1d+/- or CD1d-/- mice, unlike CD1d+/- APCs, CD1d-/- Tol-APCs failed to suppress CIA. More specifically, CD1d-/- Tol-APCs failed to suppress the production of inflammatory cytokines and the induction of Th2 responses by antigen-specific CD4 T cells both in vitro and in vivo. Our results demonstrate that the presence of CD1d-restricted NKT cells is critical for the induction of Tol-APCs-mediated suppression of CIA.


Subject(s)
Animals , Mice , Antibodies/blood , Antibody Formation/immunology , Antibody Specificity/immunology , Antigen-Presenting Cells/immunology , Antigens, CD1d/immunology , Arthritis, Experimental/blood , Collagen Type II/immunology , Cytokines/blood , Immune Tolerance/immunology , Inflammation Mediators/blood , Natural Killer T-Cells/immunology , Th1 Cells/immunology
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