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Unimpaired thymic and peripheral T cell death in mice lacking the nuclear receptor NGFI-B (Nur77).

作者信息

Lee S L, Wesselschmidt R L, Linette G P, Kanagawa O, Russell J H, Milbrandt J

机构信息

Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA.

出版信息

Science. 1995 Jul 28;269(5223):532-5. doi: 10.1126/science.7624775.

Abstract

T cell hybridomas require the immediate-early gene NGFI-B (nur77) for T cell receptor (TCR)-mediated apoptosis, a model for negative selection of self-reactive T cells. TCR-mediated death was examined in mice bearing an NGFI-B loss-of-function mutation, either by administration of antibodies to CD3 (anti-CD3) or in two well-characterized transgenic models expressing self-reactive TCRs. Both the extent and the rate of thymocyte death were unimpaired. Anti-CD3-induced death was normal in CD4+ peripheral T cells, in which death is mediated predominantly by the Fas signaling pathway. Thus, no unique requirement for NGFI-B is observed for thymic or peripheral T cell death.

摘要

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