期刊
CELL
卷 165, 期 4, 页码 827-841出版社
CELL PRESS
DOI: 10.1016/j.cell.2016.04.055
关键词
-
资金
- NIH [AI063302, AI095587, AI104914]
- Burroughs Wellcome Fund Investigator in the Pathogenesis of Infectious Disease award
- Crohn's and Colitis Foundation of America [252507]
To maintain a symbiotic relationship between the host and its resident intestinal microbiota, appropriate mucosal T cell responses to commensal antigens must be established. Mice acquire both IgG and IgA maternally; the former has primarily been implicated in passive immunity to pathogens while the latter mediates host-commensal mutualism. Here, we report the surprising observation that mice generate T cell-independent and largely Toll-like receptor (TLR)-dependent IgG2b and IgG3 antibody responses against their gut microbiota. We demonstrate that maternal acquisition of these antibodies dampens mucosal T follicular helper responses and subsequent germinal center B cell responses following birth. This work reveals a feedback loop whereby T cell-independent, TLR-dependent antibodies limit mucosal adaptive immune responses to newly acquired commensal antigens and uncovers a broader function for maternal IgG.
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