Mastitis, a common disease for female during lactation period that could cause a health risk for human or huge economic losses for animals, is mainly caused by invasion. Here, we found that neutrophil recruitment via IL-17A-mediated signaling was required for host defense against -induced mastitis in a mouse model. The rapid accumulation and activation of Vγ4 γδ T cells in the early stage of infection triggered the IL-17A-mediated immune response. Interestingly, the accumulation and influence of γδT17 cells in host defense against -induced mastitis in a commensal microbiota-dependent manner. Overall, this study, focusing on γδT17 cells, clarified innate immune response mechanisms against -induced mastitis, and provided a specific response to target for future immunotherapies. Meanwhile, a link between commensal microbiota community and host defense to mammary gland infection may unveil potential therapeutic strategies to combat these intractable infections.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10687336 | PMC |
| http://dx.doi.org/10.1016/j.isci.2023.108453 | DOI Listing |
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