Research ArticleMUCOSAL IMMUNOLOGY

Gut T cell–independent IgA responses to commensal bacteria require engagement of the TACI receptor on B cells

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Science Immunology  31 Jul 2020:
Vol. 5, Issue 49, eaat7117
DOI: 10.1126/sciimmunol.aat7117

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The second way to anti-commensal IgA

Mammals rely on secretory IgA (SIgA) at the intestinal surface to maintain a homeostatic relationship with the commensal gut microbiota. B lymphocytes differentiate into IgA-producing plasma cells through a thymus-dependent pathway that depends on B cell CD40 transducing a signal from CD40 ligand on T cells. Grasset et al. investigated the contribution of the TACI receptor found predominantly on B cells to an alternative thymus-independent (TI) pathway of IgA+ plasma cell differentiation. Mice lacking both αβ and γδ T cell subsets had no germinal centers in their lymphoid tissues but still made SIgA antibodies that bound gut bacteria through a TI mechanism requiring TACI. These findings reveal that the mucosal immune system uses parallel pathways dependent on either CD40 or TACI to provide B cells the help needed to generate SIgA capable of binding commensal bacteria.

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