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The GITR-GITRL interaction: co-stimulation or contrasuppression of regulatory activity?

Ethan M Shevach1, Geoffrey L Stephens

  • 1Cellular Immunology Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. eshevach@niaid.nih.gov

Nature Reviews. Immunology
|July 27, 2006
PubMed

Stimulation of T cells through GITR (glucocorticoid-induced tumour-necrosis-factor-receptor-related protein) has been shown to enhance immunity to tumours and viral pathogens, and to exacerbate autoimmune disease. The effects of stimulation through GITR are generally thought to be caused by attenuation of the effector activity of immunosuppressive CD4+ CD25+ regulatory T (T(Reg)) cells. Here we propose a model in which GITR-GITR-ligand interactions co-stimulate both responder T-cell functions and the suppressive functions of T(Reg) cells.

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