Journal
IMMUNITY
Volume 47, Issue 1, Pages 118-+Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2017.06.013
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Funding
- European Advanced Grant [ERC-2011-ADG-20110310]
- MINECO [SAF2014-52483-R]
- AGAUR [2014 SGR 832]
- US NIH [P01 AI61093, R01 AI57653, U01 AI95613]
- Boeringher Ingelheim [134564-2]
- NIH [R01 DK 112296-01]
- Fondo de Investigacion Sanitaria ISCIII fellowships [CD14/00060, CM13/00136]
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Secretory immunoglobulin A (SIgA) enhances host-microbiota symbiosis, whereas SIgM remains poorly understood. We found that gut IgM(+) plasma cells (PCs) were more abundant in humans than mice and clonally related to a large repertoire of memory IgM(+) B cells disseminated throughout the intestine but rare in systemic lymphoid organs. In addition to sharing a gut-specific gene signature with memory IgA(+) B cells, memory IgM(+) B cells were related to some IgA(+) clonotypes and switched to IgA in response to T cell-independent or T cell-dependent signals. These signals induced abundant IgM which, together with SIgM from clonally affiliated PCs, recognized mucus-embedded commensals. Bacteria recognized by human SIgM were dually coated by SIgA and showed increased richness and diversity compared to IgA-only-coated or uncoated bacteria. Thus, SIgM may emerge from pre-existing memory rather than newly activated naive IgM(+) B cells and could help SIgA to anchor highly diverse commensal communities to mucus.
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