Enhanced Th1 activity and development of chronic enterocolitis in mice devoid of Stat3 in macrophages and neutrophils
Enhanced Th1 activity and development of chronic enterocolitis in mice devoid of Stat3 in macrophages and neutrophils
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DOI：
10.1016/s1074-7613(00)80005-9
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发表时间：
1999-01-01
期刊：
影响因子：
32.4
通讯作者：
Akira, S
中科院分区：
文献类型：
--
作者：
Takeda, K;Clausen, BE;Akira, S
我们培育出了巨噬细胞和中性粒细胞中Stat3基因在细胞类型特异性上被破坏的小鼠。这些突变小鼠对内毒素休克高度敏感，炎症细胞因子如肿瘤坏死因子α、白细胞介素 - 1、干扰素γ和白细胞介素 - 6的产生增加。内毒素诱导的炎症细胞因子产生增加是因为白细胞介素 - 10对巨噬细胞和中性粒细胞产生炎症细胞因子的抑制作用完全被消除。这些小鼠表现出向Th1型的极化免疫反应，并随着年龄增长患上慢性小肠结肠炎。综上所述，Stat3在主要由白细胞介素 - 10介导的巨噬细胞和中性粒细胞的失活中起着关键作用。
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.