Fas and Fas ligand: lpr and gld mutations

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Abstract

Fas ligand (FasL) is a death factor that binds to its receptor, Fas, and induces apoptosis. Two mutations that accelerate autoimmune disease, lpr and gld, are known to correspond to mutations within genes encoding Fas and FasL, respectively. Here, Shigekazu Nagata and Takashi Suda summarize current knowledge of Fas and FasL, and discuss the physiological role of the Fas system in T-cell development, cytotoxicity and cytotoxic T lymphocyte (CTL)-mediated autoimmune disease.

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    We thank O. Hayaishi and C. Weissmann for encouragement and discussion. The work was carried out in collaboration with M. Adachi, J. Ogasawara, T. Takahashi, M. Tanaka, T. Kondo, M. Enari, H. Hug, N. Itoh and R. Watanabe-Fukunaga, and supported in part by Grants-in-Aid from the Ministry of Education, Science and Culture of Japan. We also thank K. Mimura for secretarial assistance.

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    Shigekazu Nagata and Takashi Suda are at the Osaka Bioscience Institute, 6-2-4 Furuedai, Suita-shi, Osaka 565, Japan.

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