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


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.

SUBMITTER: Paust S 

PROVIDER: S-EPMC478583 | biostudies-literature | 2004 Jul

REPOSITORIES: biostudies-literature

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

Paust Silke S   Lu Linrong L   McCarty Nami N   Cantor Harvey H  

Proceedings of the National Academy of Sciences of the United States of America 20040702 28


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  ...[more]

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