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J Neuroimmunol. 2019 Nov 6;338:577106. doi: 10.1016/j.jneuroim.2019.577106. [Epub ahead of print]

B cell function impacts the efficacy of IFN-β therapy in EAE.

Author information

1
Department of Arthritis and Clinical Immunology Research, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Department of Microbiology and Immunology, Oklahoma University Health Science Center, Oklahoma City, OK, USA.
2
Department of Microbiology and Immunology, Oklahoma University Health Science Center, Oklahoma City, OK, USA.
3
Department of Microbiology and Immunology, Oklahoma University Health Science Center, Oklahoma City, OK, USA. Electronic address: bob-axtell@omrf.org.

Abstract

Recent studies identified that interferon beta (IFN-β) treatment skews B-cells towards a regulatory phenotype in multiple sclerosis. To assess B cell involvement during IFN-β therapy, we compared IFN-β treatment in a B cell-independent model and a B cell-dependent model of experimental autoimmune encephalomyelitis (EAE). We show that in B cell-independent EAE, IFN-β ameliorates neuroinflammation. Conversely, in B cell-dependent EAE, IFN-β has no effect on disease. Effective IFN-β therapy in B cell-independent EAE was associated with reduced inflammatory T cells in the CNS and skewed splenic B cells towards an immature population and away from a germinal center population. These immune cell populations were unchanged in B cell-dependent EAE. Finally, we found that IFN-β increased marginal zone B cells in both EAE models. These findings indicate that B cell function impacts IFN-β efficacy during neuroinflammation.

PMID:
31715458
DOI:
10.1016/j.jneuroim.2019.577106
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