TLR and B Cell Receptor Signals to B Cells Differentially Program Primary and Memory Th1 Responses to Salmonella enterica

被引：102

作者：

Barr, Tom A. ^{[2
]}

Brown, Sheila ^{[2
]}

Mastroeni, Pietro ^{[3
]}

Gray, David ^{[1
,2
]}

机构：

[1] Univ Edinburgh, Ashworth Labs, Inst Immunol & Infect Res, Sch Biol Sci, Edinburgh EH9 3JT, Midlothian, Scotland

[2] Univ Edinburgh, Ctr Immun Infect & Evolut, Edinburgh EH9 3JT, Midlothian, Scotland

[3] Univ Cambridge, Dept Vet Med, Cambridge CB2 1TN, England

来源：

JOURNAL OF IMMUNOLOGY | 2010年 / 185卷 / 05期

基金：

英国惠康基金;

关键词：

NADPH PHAGOCYTE OXIDASE; IFN-GAMMA PRODUCTION; PRIMING IN-VIVO; CD4(+) T-CELLS; DEFICIENT MICE; SEROVAR TYPHIMURIUM; DENDRITIC CELLS; ANTIMICROBIAL ACTIONS; RHEUMATOID-ARTHRITIS; TARGETED DISRUPTION;

D O I：

10.4049/jimmunol.1001431

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Protective Th1 responses to Salmonella enterica do not develop in the absence of B cells. Using chimeric mice, we dissect the early (innate) and late (cognate) contributions of B cells to Th programming. B cell-intrinsic MyD88 signaling is required for primary effector Th1 development, whereas Ag-specific BCR-mediated Ag presentation is necessary for the development of memory Th1 populations. Programming of the primary T cell response is BCR/B cell MHC II independent, but requires MyD88-dependent secretion of cytokines by B cells. Chimeras in which B cells lack IFN-gamma or IL-6 genes make impaired Th1 or Th17 responses to Salmonella. The Journal of Immunology, 2010, 185: 2783-2789.

引用

页码：2783 / 2789

页数：7

共 67 条

[1] Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function [J].