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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 1995 Jan 31;92(3):811–815. doi: 10.1073/pnas.92.3.811

CTLA4 mediates antigen-specific apoptosis of human T cells.

J G Gribben 1, G J Freeman 1, V A Boussiotis 1, P Rennert 1, C L Jellis 1, E Greenfield 1, M Barber 1, V A Restivo Jr 1, X Ke 1, G S Gray 1, et al.
PMCID: PMC42710  PMID: 7846057

Abstract

The regulation of T cell-mediated immune responses requires a balance between amplification and generation of effector function and subsequent selective termination by clonal deletion. Although apoptosis of previously activated T cells can be induced by signaling of the tumor necrosis factor receptor family, these molecules do not appear to regulate T-cell clonal deletion in an antigen-specific fashion. We demonstrate that cross-linking of the inducible T-cell surface molecule CTLA4 can mediate apoptosis of previously activated human T lymphocytes. This function appears to be antigen-restricted, since a concomitant signal T-cell receptor signal is required. Regulation of this pathway may provide a novel therapeutic strategy to delete antigen-specific activated T cells.

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Selected References

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