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CTLA-4 control over Foxp3+ regulatory T cell function.

Author information

Affiliations

  • 1. Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan.
      Authors
    • Wing K 1
    (1 author)

ORCIDs linked to this article

Science, 01 Oct 2008, 322(5899):271-275
https://doi.org/10.1126/science.1160062 PMID: 18845758 

A comment on this article appears in "Immunology. Regulating suppression." Science. 2008 Oct 10;322(5899):202-3.

Abstract 

Naturally occurring Foxp3+CD4+ regulatory T cells (Tregs) are essential for maintaining immunological self-tolerance and immune homeostasis. Here, we show that a specific deficiency of cytotoxic T lymphocyte antigen 4 (CTLA-4) in Tregs results in spontaneous development of systemic lymphoproliferation, fatal T cell-mediated autoimmune disease, and hyperproduction of immunoglobulin E in mice, and it also produces potent tumor immunity. Treg-specific CTLA-4 deficiency impairs in vivo and in vitro suppressive function of Tregs-in particular, Treg-mediated down-regulation of CD80 and CD86 expression on dendritic cells. Thus, natural Tregs may critically require CTLA-4 to suppress immune responses by affecting the potency of antigen-presenting cells to activate other T cells.

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Read article at publisher's site: https://doi.org/10.1126/science.1160062

Free to read at www.sciencemag.org
http://www.sciencemag.org/cgi/content/abstract/322/5899/271

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http://www.sciencemag.org/cgi/content/full/322/5899/271

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