Journal
CELL
Volume 176, Issue 3, Pages 610-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2018.11.035
Keywords
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Categories
Funding
- Canadian Institutes of Health Research [CIHR 388337]
- Tier 2 Canadian Research Chair in Mucosal Immunology
- MS Society of Canada Research Foundation
- Tier 1 Canada Research Chair in Multiple Sclerosis
- Swiss National Science Foundation fellowship [P2SKP3_164938/1, P300PB_177927/1]
- National Multiple Sclerosis Society fellowship (NMSS Kathleen C. Moore Fellowship) [FG-1708-28871]
- NIH [R01-AI113543, AI085043SSZ, RO1 NS092835, R21 NS108159-01]
- Canadian Institutes of Health Research (CIHR) Foundation [FDN148386]
- NMSS [RG1701-26628]
- Maisin Foundation
- Biogen
- Celgene
- US National MS Society [CA1072-A-7]
- US Department of Defense [W81XWH-15-1-0652]
- Valhalla Charitable Foundation
- CIHR Foundation grant [FDN1552]
- MS Society of Canada grant [EGID3194]
- Swiss National Science Foundation (SNF) [P2SKP3_164938, P300PB_177927] Funding Source: Swiss National Science Foundation (SNF)
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Plasma cells (PC) are found in the CNS of multiple sclerosis (MS) patients, yet their source and role in MS remains unclear. We find that some PC in the CNS of mice with experimental autoimmune encephalomyelitis (EAE) originate in the gut and produce immunoglobulin A (IgA). Moreover, we show that IgA(+) PC are dramatically reduced in the gut during EAE, and likewise, a reduction in IgA-bound fecal bacteria is seen in MS patients during disease relapse. Removal of plasmablast (PB) plus PC resulted in exacerbated EAE that was normalized by the introduction of gut-derived IgA(+) PC. Furthermore, mice with an over-abundance of IgA(+) PB and/or PC were specifically resistant to the effector stage of EAE, and expression of interleukin (IL)-10 by PB plus PC was necessary and sufficient to confer resistance. Our data show that IgA(+) PB and/or PC mobilized from the gut play an unexpected role in suppressing neuroinflammation.
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