Nature immunology, 2002-02, Vol.3 (2), p.135-142
2002
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Details
- Autor(en) / Beteiligte
- Titel
- Stimulation of CD25 + CD4 + regulatory T cells through GITR breaks immunological self-tolerance
- Ist Teil von
- Nature immunology, 2002-02, Vol.3 (2), p.135-142
- Ort / Verlag
- United States: Nature Publishing Group
- Erscheinungsjahr
- 2002
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1529-2908eISSN: 1529-2916DOI: 10.1038/ni759Titel-ID: cdi_proquest_miscellaneous_71407504
- Format
- –
- Schlagworte
- Animals, Autoimmune diseases, Autoimmune Diseases - etiology, CD4 Antigens - isolation & purification, CD4-Positive T-Lymphocytes - immunology, Dimerization, Glucocorticoid-Induced TNFR-Related Protein, Glycoproteins - antagonists & inhibitors, Glycoproteins - immunology, Glycoproteins - metabolism, Immune Tolerance - immunology, Lymph Nodes - immunology, Mice, Mice, Inbred BALB C, Rats, Rats, Wistar, Receptors, Interleukin-2 - isolation & purification, Receptors, Nerve Growth Factor - antagonists & inhibitors, Receptors, Nerve Growth Factor - immunology, Receptors, Nerve Growth Factor - metabolism, Receptors, Tumor Necrosis Factor - antagonists & inhibitors, Receptors, Tumor Necrosis Factor - immunology, Receptors, Tumor Necrosis Factor - metabolism, Signal Transduction, Spleen - immunology, T-Lymphocyte Subsets - immunology, Tumors