You are currently viewing the abstract.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
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.
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.
- Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works
This is an article distributed under the terms of the Science Journals Default License.