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Recirculating Intestinal IgA-Producing Cells Regulate Neuroinflammation via IL-10
Olga L. Rojas ,
Anne-Katrin Pröbstel ,
Elisa A. Porfilio ,
Angela A. Wang ,
Marc Charabati ,
Tian Sun ,
Dennis S.W. Lee ,
Georgina Galicia ,
Valeria Ramaglia ,
Lesley A. Ward ,
Leslie Y.T. Leung ,
Ghazal Najafi ,
Khashayar Khaleghi ,
Beatriz Garcillán ,
Angela Li ,
Rickvinder Besla ,
Ikbel Naouar ,
Eric Y. Cao ,
Pailin Chiaranunt ,
Kyle Burrows ,
Hannah G. Robinson ,
Jessica R. Allanach ,
Jennifer Yam ,
Helen Luck ,
Daniel J. Campbell ,
David Allman ,
David G. Brooks ,
Michio Tomura ,
Ryan Baumann ,
Scott S. Zamvil ,
Amit Bar-Or ,
Marc S. Horwitz ,
Daniel A. Winer ,
Arthur Mortha ,
Fabienne Mackay ,
Alexandre Prat ,
Lisa C. Osborne ,
Clinton Robbins ,
Sergio E. Baranzini ,
Jennifer L. Gommerman
January 2019
January 2019
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Abstract
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) and/or 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 and/or 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.