The role of innate-like B1 cells in the regulation of sex-dependent immune responses to Chlamydia infection
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Chlamydia infections predominantly impact women’s health and the biological basis underlying the sex-dependent disparity is unclear. I demonstrate that female mice are significantly more susceptible to respiratory Chlamydia infection than their male counterparts, indicated by significantly greater body weight loss and higher bacterial loads. Furthermore, female mice produce more Chlamydia-specific antibodies, whereas male mice generate robust IFN-ɤ-mediated cellular immunity, but less IL-10- and IL-13-mediated responses. Remarkably, female mice have inherently more innate B1 cells, which migrate to the lungs and draining lymph nodes upon Chlamydia infection in vivo. Finally, I demonstrate that B1 cells, particularly the ones from female mice, produce a large quantity of IL-10 upon Chlamydia stimulation and potently induce inhibitory regulatory CD4 T cells differentiation in vitro. Together, I show that male and female mice are inherently different in B1 cells, which play a key role in host susceptibility to Chlamydia infection by regulating T cell responses.