Essential role of LAT in T cell development

被引：474

作者：

Zhang, WG

Sommers, CL

Burshtyn, DN

Stebbins, CC

DeJarnette, JB

Trible, RP

Grinberg, A

Tsay, HC

Jacobs, HM

Kessler, CM

Long, EO

Love, PE

Samelson, LE ^{[1
]}

机构：

[1] NICHHD, Sect Lymphocyte Signaling, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA

[2] NICHHD, Lab Mammalian Genes & Dev, NIH, Bethesda, MD 20892 USA

[3] NIAID, Immunogenet Lab, NIH, Bethesda, MD 20892 USA

[4] Georgetown Univ, Med Ctr, Vincent T Lombardi Canc Res Ctr, Div Hematol Oncol, Washington, DC 20007 USA

来源：

IMMUNITY | 1999年 / 10卷 / 03期

基金：

英国医学研究理事会;

关键词：

D O I：

10.1016/S1074-7613(00)80032-1

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The linker molecule LAT is a substrate of the tyrosine kinases activated following TCR engagement. Phosphorylated LAT binds many critical signaling molecules. The central role of this molecule in TCR-mediated signaling has been demonstrated by experiments in a LAT-deficient cell line. To probe the role of LAT in T cell development, the LAT gene was disrupted by targeting. LAT-deficient mice appeared healthy. Flow cytometric analysis revealed normal B cell populations but the absence of any mature peripheral T cells. Intra; thymic development was blocked within the CD4(-)CD8(-) stage. No gross abnormality of NK or platelet function was observed. LAT is thus critical to both T cell activation and development.

引用

页码：323 / 332

页数：10

共 55 条

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