Gut T cell–independent IgA responses to commensal bacteria require engagement of the TACI receptor on B cells
- 3 July 2020
- journal article
- research article
- Published by American Association for the Advancement of Science (AAAS) in Science Immunology
- Vol. 5 (49)
- https://doi.org/10.1126/sciimmunol.aat7117
Abstract
The gut mounts secretory immunoglobulin A (SIgA) responses to commensal bacteria through nonredundant T cell–dependent (TD) and T cell–independent (TI) pathways that promote the establishment of mutualistic host-microbiota interactions. SIgAs from the TD pathway target penetrant bacteria, and their induction requires engagement of CD40 on B cells by CD40 ligand on T follicular helper cells. In contrast, SIgAs from the TI pathway bind a larger spectrum of bacteria, but the mechanism underpinning their production remains elusive. Here, we show that the intestinal TI pathway required CD40-independent B cell–activating signals from TACI, a receptor for the innate CD40 ligand–like factors BAFF and APRIL. TACI-induced SIgA responses targeted a fraction of the gut microbiota without shaping its overall composition. Of note, TACI was dispensable for TD induction of IgA in gut-associated lymphoid organs. Thus, BAFF/APRIL signals acting on TACI orchestrate commensal bacteria–specific SIgA responses through an intestinal TI program.Keywords
Funding Information
- National Institutes of Health (P01 AI61093)
- Ministerio de Ciencia, Innovación y Universidades (RTI2018-093894-B-I00)
- European Research Council (ERC-2011-ADG-20110310)
- the Kenneth Rainin Foundation (Innovator Award 2015-936)
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