MyD88 signaling in T cells directs IgA-mediated control of the microbiota to promote health

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Abstract

Altered commensal communities are associated with human disease. IgA mediates intestinal homeostasis and regulates microbiota composition. Intestinal IgA is produced at high levels as a result of T follicular helper cell (TFH) and B cell interactions in germinal centers. However, the pathways directing host IgA responses toward the microbiota remain unknown. Here, we report that signaling through the innate adaptor MyD88 in gut T cells coordinates germinal center responses, including TFH and IgA+ B cell development. TFH development is deficient in germ-free mice and can be restored by feeding TLR2 agonists that activate T cell-intrinsic MyD88 signaling. Loss of this pathway diminishes high-affinity IgA targeting of the microbiota and fails to control the bacterial community, leading to worsened disease. Our findings identify that T cells converge innate and adaptive immune signals to coordinate IgA against the microbiota, constraining microbial community membership to promote symbiosis.

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Kubinak, J. L., Petersen, C., Stephens, W. Z., Soto, R., Bake, E., O’Connell, R. M., & Round, J. L. (2015). MyD88 signaling in T cells directs IgA-mediated control of the microbiota to promote health. Cell Host and Microbe, 17(2), 153–163. https://doi.org/10.1016/j.chom.2014.12.009

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