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Development of Stem Cell-derived Antigen-specific Regulatory T Cells Against Autoimmunity
Published on: November 8, 2016
Superantigen-induced regulatory T cells in vivo
1Section for Immunology, Lund University, Lund, Sweden.
Bacterial and viral superantigens (SAgs) can induce the activation of a large fraction of the T cells in an individual. The activated T cells divide and produce a strong cytokine response. Subsequently, the majority of the expanded T cells are deleted and the remaining SAg-reactive cells will be anergic and tolerant to SAg exposure. The anergic population is heterogeneous and includes both T cells with induced nonresponsiveness to the SAg and SAg-specific regulatory T cells (Tregs). Both CD4+CD25- and CD4+CD25+ Tregs are generated in SAg-induced responses. The Tregs suppress T cell activation and produce the immunosuppressive cytokines IL-10 and TGF-Beta1, thereby contributing to the SAg-specific tolerance. The similarities of immune responses induced by SAgs and conventional peptide antigens administered in the absence of adjuvants will be discussed. It is proposed that the antigen-specific tolerance induced in both situations is the consequence of T cell activation mediated by immature dendritic cells.
Bacterial and viral superantigens (SAgs) can induce the activation of a large fraction of the T cells in an individual. The activated T cells divide and produce a strong cytokine response. Subsequently, the majority of the expanded T cells are deleted and the remaining SAg-reactive cells will be anergic and tolerant to SAg exposure. The anergic population is heterogeneous and includes both T cells with induced nonresponsiveness to the SAg and SAg-specific regulatory T cells (Tregs). Both CD4+CD25- and CD4+CD25+ Tregs are generated in SAg-induced responses. The Tregs suppress T cell activation and produce the immunosuppressive cytokines IL-10 and TGF-Beta1, thereby contributing to the SAg-specific tolerance. The similarities of immune responses induced by SAgs and conventional peptide antigens administered in the absence of adjuvants will be discussed. It is proposed that the antigen-specific tolerance induced in both situations is the consequence of T cell activation mediated by immature dendritic cells.

