T cells express a phagocyte-type NADPH oxidase that is activated after T cell receptor stimulation

被引：379

作者：

Jackson, SH

Devadas, S

Kwon, J

Pinto, LA

Williams, MS

机构：

[1] NIAID, Host Def Lab, NIH, Bethesda, MD 20892 USA

[2] Amer Red Cross, Dept Immunol, Rockville, MD 20855 USA

[3] Sci Applicat Int Corp, Natl Canc Inst, Frederick, MD 21702 USA

来源：

NATURE IMMUNOLOGY | 2004年 / 5卷 / 08期

关键词：

D O I：

10.1038/ni1096

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

T cell receptor (TCR) stimulation induces rapid generation of reactive oxygen species, although the mechanisms for this are unclear. Here we found that T cells expressed a functional phagocyte-type nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. TCR crosslinking induced oxidase activation through the recruitment of preformed Fas ligand and Fas. TCR stimulation induced three separable events generating reactive oxygen species: rapid hydrogen peroxide production independent of Fas or NADPH oxidase; sustained hydrogen peroxide production dependent on both Fas and NADPH oxidase; and delayed superoxide production that was dependent on Fas ligand and Fas yet independent of NADPH oxidase. NADPH oxidase-deficient T cells showed enhanced activation of the kinase Erk and a relative increase in T helper type 1 cytokine secretion. Thus, mature T cells express a phagocyte-type NADPH oxidase that regulates elements of TCR signaling.

引用

收藏

页码：818 / 827

页数：10

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