IMR Press / FBL / Volume 11 / Issue 1 / DOI: 10.2741/1848

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Signal transduction in CD4+CD25+ regulatory T cells: CD25 and IL-2

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1 Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 USA
Front. Biosci. (Landmark Ed) 2006, 11(1), 921–927;
Published: 1 January 2006

IL-2 was originally identified as a growth factor critical for T cell proliferation in vitro. Although the early studies of IL-2 strongly implied an obligate role of IL-2 in T cell growth, it was later shown that mice deficient in IL-2 or in IL-2R developed an unexpected lymphocytic hyperproliferation and subsequent autoimmune disease. In separate studies of autoimmunity, it was observed that a population of CD4+ T cells suppressed the induction of autoimmunity in several in vivo models of autoimmune disease. It was not until the characterization of this subpopulation of CD4+ T cells demonstrated that they co-expressed the IL-2R-alpha chain (CD25) that the puzzling phenotype observed in IL-2 deficient mice began to be truly explained. The constitutive expression of the IL-2R-alpha chain on CD4+CD25+ T cells led to the obvious speculation that IL-2 signaling in CD4+CD25+ T cells was important to these cells. Recent studies have examined the role of IL-2 in the generation, the expansion, the survival and the effector function of CD4+CD25+ T cells. It is now evident that IL-2 is critical for the development of CD4+CD25+ T cells and the phenotype observed in IL-2 and IL-2R deficient mice is most readily explained by the absence of these potent suppressors.

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