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Proc Natl Acad Sci U S A. 2004 Jul 13;101(28):10398-403. Epub 2004 Jul 2.

Engagement of B7 on effector T cells by regulatory T cells prevents autoimmune disease.

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  • 1Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School, 44 Binney Street, SM 722, Boston, MA 02115, USA.

Abstract

Although there is considerable evidence that a subpopulation of regulatory CD4(+)CD25+ T cells can suppress the response of autoreactive T cells, the underlying molecular mechanism is not understood. We find that transmission of a suppressive signal by CD4CD25+ regulatory cells requires engagement of the B7 molecule expressed on target T cells. The response of T cells from B7-deficient mice is resistant to suppression in vitro, and these cells provoke a lethal wasting disease in lymphopenic mice despite the presence of regulatory T cells. Susceptibility of B7-deficient cells to suppression is restored by lentiviral-based expression of full-length, but not truncated, B7 lacking a transmembrane/cytoplasmic domain. Because expression of these B7 truncation mutants restores CD28-dependent costimulatory activity, these findings that indicate B7-based transmission of suppressive activity suggest new approaches to modifying autoimmune responses.

PMID:
15235129
[PubMed - indexed for MEDLINE]
PMCID:
PMC478583
Free PMC Article
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