期刊
CELL HOST & MICROBE
卷 17, 期 2, 页码 153-163出版社
CELL PRESS
DOI: 10.1016/j.chom.2014.12.009
关键词
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资金
- National Center for Research Resources of the National Institutes of Health [1S10RR026802-01]
- UNC's Gnotobiotic Facility [5-P39-DK034987, 5-P40-OD010995]
- T32 fellowship in microbial pathogenesis [AI-055434]
- T32 genetics training grant [GM007464]
- NIH [DP2GM111099-01, DP2AT008746-01]
- NHLBI [R00HL102228-05]
- American Cancer Society Research
- Kimmel Scholar Award
- NIAID [AI107090, AI109122]
- Edward Mallinckrodt Jr. Foundation
- Pew Scholars Program
- NSF CAREER award [IOS-1253278]
- Packard Fellowship in Science and Engineering
- NIAID K22 [AI95375]
Altered commensal communities are associated with human disease. IgA mediates intestinal homeostasis and regulates microbiota composition. Intestinal IgA is produced at high levels as a result of T follicular helper cell (T-FH) and B cell interactions in germinal centers. However, the pathways directing host IgA responses toward the microbiota remain unknown. Here, we report that signaling through the innate adaptor MyD88 in gut T cells coordinates germinal center responses, including TFH and IgA+ B cell development. TFH development is deficient in germfree mice and can be restored by feeding TLR2 agonists that activate T cell-intrinsic MyD88 signaling. Loss of this pathway diminishes high-affinity IgA targeting of the microbiota and fails to control the bacterial community, leading to worsened disease. Our findings identify that T cells converge innate and adaptive immune signals to coordinate IgA against the microbiota, constraining microbial community membership to promote symbiosis.
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