期刊
IMMUNITY
卷 41, 期 3, 页码 478-492出版社
CELL PRESS
DOI: 10.1016/j.immuni.2014.08.009
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资金
- NIH [HHSN272201400004C, U19AI090023, U54AI057157, R37AI48638, R37DK057665, U19AI057266, AI100663-02, DK099071, DK083890, AI085263, P40 OD010995, P30 DK34987]
- Bill and Melinda Gates Foundation
- Crohn's and Colitis Foundation of America
- Burroughs Wellcome Fund
- Influenza Pathogenesis and Immunology Research Center - CEIRS
Systems biological analysis of immunity to the trivalent inactivated influenza vaccine (TIV) in humans revealed a correlation between early expression of TLR5 and the magnitude of the antibody response. Vaccination of Trl5(-/-) mice resulted in reduced antibody titers and lower frequencies of plasma cells, demonstrating a role for TLR5 in immunity to TIV. This was due to a failure to sense host microbiota. Thus, antibody responses in germ-free or antibiotic-treated mice were impaired, but restored by oral reconstitution with a flagellated, but not aflagellated, strain of E. coli. TLR5-mediated sensing of flagellin promoted plasma cell differentiation directly and by stimulating lymph node macrophages to produce plasma cell growth factors. Finally, TLR5-mediated sensing of the microbiota also impacted antibody responses to the inactivated polio vaccine, but not to adjuvanted vaccines or the live-attenuated yellow fever vaccine. These results reveal an unappreciated role for gut microbiota in promoting immunity to vaccination.
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