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      Stimulation of CD25(+)CD4(+) regulatory T cells through GITR breaks immunological self-tolerance.

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          Abstract

          CD25(+)CD4(+) regulatory T cells in normal animals are engaged in the maintenance of immunological self-tolerance. We show here that glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR, also known as TNFRSF18)--a member of the tumor necrosis factor-nerve growth factor (TNF-NGF) receptor gene superfamily--is predominantly expressed on CD25(+)CD4(+) T cells and on CD25(+)CD4(+)CD8(-) thymocytes in normal naïve mice. We found that stimulation of GITR abrogated CD25(+)CD4(+) T cell-mediated suppression. In addition, removal of GITR-expressing T cells or administration of a monoclonal antibody to GITR produced organ-specific autoimmune disease in otherwise normal mice. Thus, GITR plays a key role in dominant immunological self-tolerance maintained by CD25(+)CD4(+) regulatory T cells and could be a suitable molecular target for preventing or treating autoimmune disease.

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          Author and article information

          Journal
          Nat Immunol
          Nature immunology
          Springer Science and Business Media LLC
          1529-2908
          1529-2908
          Feb 2002
          : 3
          : 2
          Affiliations
          [1 ] Department of Immunopathology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan.
          Article
          ni759
          10.1038/ni759
          11812990
          ea9994ce-26cd-4770-abea-f29a10b8f6cb

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