Authors
Olga L Rojas, Anne-Katrin Pröbstel, Elisa A Porfilio, Angela A Wang, Marc Charabati, Tian Sun, Dennis SW Lee, Georgina Galicia, Valeria Ramaglia, Lesley A Ward, Leslie YT 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
Publication date
2019/1/24
Journal
Cell
Volume
176
Issue
3
Pages
610-624. e18
Publisher
Elsevier
Description
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 …
Scholar articles
OL Rojas, AK Pröbstel, EA Porfilio, AA Wang… - Cell, 2019