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

Nature Reviews Immunology volume 6, pages 613–618 (2006)Cite this article

Abstract

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 (TReg) cells. Here we propose a model in which GITR–GITR-ligand interactions co-stimulate both responder T-cell functions and the suppressive functions of TReg cells.

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Figure 1: Initial hypothesis concerning the effects of GITR signalling on TReg cells.
Figure 2: Model of GITR–GITRL interaction dynamics during an immune response.
Figure 3: Boosting responder T-cell function and enhancing resistance to TReg-cell-mediated suppression.

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  1. the Cellular Immunology Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, 20892, Maryland, USA

    Ethan M. Shevach & Geoffrey L. Stephens

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  1. Ethan M. Shevach
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Correspondence to Ethan M. Shevach.

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Shevach, E., Stephens, G. The GITR–GITRL interaction: co-stimulation or contrasuppression of regulatory activity?. Nat Rev Immunol 6, 613–618 (2006). https://doi.org/10.1038/nri1867

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