期刊
JOURNAL OF IMMUNOLOGY
卷 189, 期 8, 页码 3800-3804出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1103080
关键词
-
类别
资金
- National Institutes of Health [R01 AI079065, R01 AI05609, R01 HL45635]
- Indiana Clinical and Translational Sciences Institute
- Center of Excellence in Molecular Hematology at Indiana University [NIDDK P30 DK090948]
- Children's Discovery Institute at Washington University and St. Louis Children's Hospital
- American Heart Association
Phagocyte NADPH oxidase plays a key role in pathogen clearance via reactive oxygen species (ROS) production. Defects in oxidase function result in chronic granulomatous disease with hallmark recurrent microbial infections and inflammation. The oxidase's role in the adaptive immune response is not well understood. Class II presentation of cytoplasmic and exogenous Ag to CD4(+) T cells was impaired in human B cells with reduced oxidase p40(phox) subunit expression. Naturally arising mutations, which compromise p40(phox) function in a chronic granulomatous disease patient, also perturbed class II Ag presentation and intracellular ROS production. Reconstitution of patient B cells with a wild-type, but not a mutant, p40(phox) allele restored exogenous Ag presentation and intracellular ROS generation. Remarkably, class II presentation of epitopes from membrane Ag was robust in p40(phox) -deficient B cells. These studies reveal a role for NADPH oxidase and p40(phox) in skewing epitope selection and T cell recognition of self Ag. The Journal of Immunology, 2012, 189:3800-3804.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据