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• W119240209 endingPage "117" @default.
• W119240209 startingPage "101" @default.
• W119240209 abstract "Many escape mechanisms have been proposed to explain the failure of the immune system to detect and reject tumor cells. The identification of Fas ligands on the surface of multiple types of tumor cells has led to the recognition that tumor cells may escape destruction by immune effector cells, and may be actively involved in the killing of Fas-expressing lymphocytes. Thus, the Fas/Fas ligand (Fas/FasL) interaction serves both as a mechanism of cytotoxicity for T and natural killer (NK) cells, and as a tumor “counterattack” mechanism against lymphocytes. This mechanism of tumor-induced death of infiltrating lymphocytes complements the concept of FasL-mediating immune-privilege to certain organs, such as the eye, testes, or ovary, where histocompatibility differences are partially tolerated. Despite the wealth of data supporting the role of the Fas/FasL system in mediating immune-privilege and tumor counterattack, these concepts have recently been challenged by many contradictory reports. Here, we review the evidence for and against a role for the Fas/FasL system in immune escape mechanisms." @default.
• W119240209 created "2016-06-24" @default.
• W119240209 creator A5022074466 @default.
• W119240209 creator A5087859996 @default.
• W119240209 date "2004-01-01" @default.
• W119240209 modified "2023-09-23" @default.
• W119240209 title "The Role of Receptor-Mediated Apoptosis in T-Cell Dysfunction" @default.
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