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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.
•Report on the impact of microbiome on vaccine immunity•Example of a novel insight obtained from a systems vaccinology study in human•New role for microbiome on modulating short- and long-lived plasma cell responses•New insight on the regulation of immunity to influenza vaccine
Emerging evidence suggests diverse roles for the host microbiota in human physiology. Pulendran and colleagues show that the microbiota signal via TLR5 on B cells and macrophages to promote antibody responses to vaccination.