UNIMPAIRED THYMIC AND PERIPHERAL T-CELL DEATH IN MICE LACKING THE NUCLEAR RECEPTOR NGFI-B (NUR77)

被引:233
作者
LEE, SL
WESSELSCHMIDT, RL
LINETTE, GP
KANAGAWA, O
RUSSELL, JH
MILBRANDT, J
机构
[1] WASHINGTON UNIV, SCH MED, DEPT PATHOL, HOWARD HUGHES MED INST, ST LOUIS, MO 63110 USA
[2] WASHINGTON UNIV, SCH MED, DEPT INTERNAL MED, ST LOUIS, MO 63110 USA
[3] WASHINGTON UNIV, JEWISH HOSP ST LOUIS, SCH MED, DEPT MED, ST LOUIS, MO 63110 USA
[4] WASHINGTON UNIV, JEWISH HOSP ST LOUIS, SCH MED, DEPT GENET, ST LOUIS, MO 63110 USA
[5] WASHINGTON UNIV, SCH MED, DEPT MED, ST LOUIS, MO 63110 USA
[6] WASHINGTON UNIV, SCH MED, DEPT MOLEC BIOL & PHARMACOL, ST LOUIS, MO 63110 USA
关键词
D O I
10.1126/science.7624775
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页码:532 / 535
页数:4
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