AN ACTIVATED LCK TRANSGENE PROMOTES THYMOCYTE DEVELOPMENT IN RAG-1 MUTANT MICE

被引：150

作者：

MOMBAERTS, P

ANDERSON, SJ

PERLMUTTER, RM

MAK, TW

TONEGAWA, S

机构：

[1] MIT,HOWARD HUGHES MED INST,CAMBRIDGE,MA 02139

[2] MIT,CTR CANC RES,DEPT BIOL,CAMBRIDGE,MA 02139

[3] UNIV WASHINGTON,DEPT IMMUNOL,SEATTLE,WA 98185

[4] UNIV WASHINGTON,DEPT BIOCHEM,SEATTLE,WA 98185

[5] UNIV WASHINGTON,DEPT MED MED GENET,SEATTLE,WA 98185

[6] UNIV TORONTO,AMGEN INST,ONTARIO CANC INST,DEPT IMMUNOL,TORONTO M4X 1K9,ON,CANADA

[7] UNIV TORONTO,DEPT MED BIOPHYS,TORONTO M4X 1K9,ON,CANADA

来源：

IMMUNITY | 1994年 / 1卷 / 04期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1016/1074-7613(94)90077-9

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Expression of the T cell receptor P (TCR beta) chain is necessary for the transition from the CD4(-)CD8(-) stage in the major alpha beta thymocyte lineage. The protein tyrosine kinase p56(lck) has been implicated in the regulation of early thymocyte differentiation and of allelic exclusion at the TCR beta locus. Using mice overexpressing an activated lck transgene and mice with a disruption of the lck gene, we demonstrate that p5(lck) participates in a pathway that regulates the expansion of the pool of CD4(+)CD8(+) thymocytes to wild-type levels. In addition, p56(lck) may be involved in the down-regulation of the putative pre-TCR on CD4(+)CD8(+) thymocytes.

引用

页码：261 / 267

页数：7

共 42 条

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ABRAHAM KM, 1992, J EXP MED, V175, P1421

[2] INVOLVEMENT OF THE PROTEIN-TYROSINE KINASE P56(LCK) IN T-CELL SIGNALING AND THYMOCYTE DEVELOPMENT [J].