APOPTOSIS, FAS AND SYSTEMIC AUTOIMMUNITY - THE MRL-IPR/IPR MODEL

被引：132

作者：

SINGER, GG ^{[5
]}

CARRERA, AC

MARSHAKROTHSTEIN, A

MARTINEZA, C

ABBAS, AK

机构：

[1] BRIGHAM & WOMENS HOSP, DEPT MED, DIV RENAL, BOSTON, MA 02115 USA

[2] HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA

[3] UNIV AUTONOMA MADRID, CTR NACL BIOTECNOL, E-28049 MADRID, SPAIN

[4] BOSTON UNIV, SCH MED, DEPT MICROBIOL & IMMUNOL, BOSTON, MA 02109 USA

[5] BRIGHAM & WOMENS HOSP, DEPT PATHOL, DIV IMMUNOL RES, BOSTON, MA 02155 USA

[6] HARVARD UNIV, SCH MED, BOSTON, MA 02155 USA

来源：

CURRENT OPINION IN IMMUNOLOGY | 1994年 / 6卷 / 06期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1016/0952-7915(94)90013-2

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Proteins encoded by the fas and fas ligand (fasL) genes are involved in apoptotic cell death in lymphocytes. In this article we review the recent elucidation of the role of the Fas-FasL interactions in the maintenance of tolerance to self antigens and in the homeostatic regulation of lymphocyte clonal expansion, and discuss the mechanisms of autoimmunity in Fas- and FasL-deficient mutant mouse strains.

引用

页码：913 / 920

页数：8

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