Gut T cell-independent IgA responses to commensal bacteria require engagement of the TACI receptor on B cells.
Animals
B-Lymphocytes
/ immunology
Bacteria
/ genetics
Gastrointestinal Microbiome
Gastrointestinal Tract
/ immunology
Immunity, Mucosal
Immunoglobulin A
/ genetics
Mice
Mice, Inbred C57BL
Mice, Knockout
RNA, Ribosomal, 16S
/ genetics
T-Lymphocytes
Transmembrane Activator and CAML Interactor Protein
/ immunology
Journal
Science immunology
ISSN: 2470-9468
Titre abrégé: Sci Immunol
Pays: United States
ID NLM: 101688624
Informations de publication
Date de publication:
31 07 2020
31 07 2020
Historique:
received:
27
03
2018
accepted:
09
07
2020
entrez:
2
8
2020
pubmed:
2
8
2020
medline:
11
1
2022
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 32737068
pii: 5/49/eaat7117
doi: 10.1126/sciimmunol.aat7117
pmc: PMC8349226
mid: NIHMS1641292
pii:
doi:
Substances chimiques
Immunoglobulin A
0
RNA, Ribosomal, 16S
0
Transmembrane Activator and CAML Interactor Protein
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIAID NIH HHS
ID : K23 AI137183
Pays : United States
Organisme : NIAID NIH HHS
ID : P01 AI061093
Pays : United States
Informations de copyright
Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
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