Enhanced Th1 activity and development of chronic enterocolitis in mice devoid of Stat3 in macrophages and neutrophils

被引：1035

作者：

Takeda, K

Clausen, BE

Kaisho, T

Tsujimura, T

Terada, N

Förster, I

Akira, S

机构：

[1] Hyogo Coll Med, Dept Biochem, Nishinomiya, Hyogo 6638501, Japan

[2] Hyogo Coll Med, Dept Pathol, Nishinomiya, Hyogo 6638501, Japan

[3] Univ Cologne, Inst Genet, D-50931 Cologne, Germany

[4] Japan Sci & Technol Corp, Core Res Evolut Sci & Technol, Chiyoda Ku, Tokyo 1010062, Japan

来源：

IMMUNITY | 1999年 / 10卷 / 01期

关键词：

D O I：

10.1016/S1074-7613(00)80005-9

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

We have generated mice with a cell type-specific disruption of the Stat3 gene in macrophages and neutrophils, The mutant mice are highly susceptible to endotoxin shock with increased production of inflammatory cytokines such as TNF alpha, IL-1, IFN gamma, and IL-6. Endotoxin-induced production of inflammatory cytokines is augmented because the suppressive effects of IL-10 on inflammatory cytokine production from macrophages and neutrophils are completely abolished. The mice show a polarized immune response toward the Th1 type and develop chronic enterocolitis with age. Taken together, Stat3 plays a critical role in deactivation of macrophages and neutrophils mainly exerted by IL-10.

引用

页码：39 / 49

页数：11

共 39 条

[1] MOLECULAR TRANSDUCTIONAL MECHANISMS BY WHICH IFN-GAMMA AND OTHER SIGNALS REGULATE MACROPHAGE DEVELOPMENT [J].