Regulation of the proinflammatory effects of Fas ligand (CD95L)

被引：308

作者：

Chen, JJ

Sun, YN

Nabel, GJ

机构：

[1] Univ Michigan, Med Ctr, Dept Internal Med, Howard Hughes Med Inst, Ann Arbor, MI 48109 USA

[2] Univ Michigan, Med Ctr, Dept Biol Chem, Howard Hughes Med Inst, Ann Arbor, MI 48109 USA

来源：

SCIENCE | 1998年 / 282卷 / 5394期

关键词：

D O I：

10.1126/science.282.5394.1714

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：

Fas ligand (CD95L) inhibits T cell function in immune-privileged organs such as the eye and testis, yet in most tissues CD95L expression induces potent inflammatory responses. With a stably transfected colon carcinoma cell Line, CT26-CD95L, the molecular basis for these divergent responses was defined. When injected subcutaneously, rejection of CT26-CD95L was caused by neutrophils activated by CD95L. CT26-CD95L survived in the intraocular space because of the presence of transforming growth factor-beta (TGF-beta), which inhibited neutrophil activation. Providing TGF-beta to subcutaneous sites protected against tumor rejection. Thus, these cytokines together generate a microenvironment that promotes immunologic tolerance, which may aid in the amelioration of allograft rejection.

引用

页码：1714 / 1717

页数：4

共 38 条

[21] Prevention of islet allograft rejection with engineered myoblasts expressing FasL in mice [J].