CTLA4 mediates antigen-specific apoptosis of human T cells.

作者：John G. Gribben, Gordon James Freeman, Vassiliki A. Boussiotis, Paul D. Rennert, C L Jellis, Edward A. Greenfield, Melissa A. Barber, Vincent A. Restivo, Xiao-Yen Ke, G S Gray · 发表于：Proceedings of the National Academy of Sciences · 年份：1995 · DOI：10.1073/pnas.92.3.811 · 被引用次数：322 · 研究领域：T-cell and B-cell Immunology、Monoclonal and Polyclonal Antibodies Research、Immunotherapy and Immune Responses

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.