Journal
NEUROLOGY-NEUROIMMUNOLOGY & NEUROINFLAMMATION
Volume 7, Issue 3, Pages -Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/NXI.0000000000000698
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Funding
- VorSPrUNG program of the UMG
- US NIH [1 RO1 NS092835-01, 1 R01 AI131624-01A1, 1 R21 NS108159-01, 1 R21AI142186-01A1]
- US National Multiple Sclerosis Society [1 RG1701-26628]
- Weill Institute
- Maisin Foundation
- Swiss National Science Foundation [SNSF_ 310030_ 176078]
- National Multiple Sclerosis Society (NMSS) [PP 1660]
- Deutsche Forschungsgemeinschaft (DFG) [WE 3547/5-1]
- Novartis
- Teva
- Biogen Idec
- Roche
- Merck
- ProFutura Programm of the UMG
- Startprogramm of the UMG
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Objective We examined the effect of glatiramer acetate (GA) on B-cell maturation, differentiation, and antigen presentation in MS and experimental autoimmune encephalomyelitis (EAE). Methods A cross-sectional study of blood samples from 20 GA-treated and 18 untreated patients with MS was performed by flow cytometry; 6 GA-treated patients with MS were analyzed longitudinally. GA-mediated effects on B-cell antigen-presenting function were investigated in EAE, or, alternatively, B cells were treated with GA in vitro using vehicle as a control. Results In MS, GA diminished transitional B-cell and plasmablast frequency, downregulated CD69, CD25, and CD95 expression, and decreased TNF-alpha production, whereas IL-10 secretion and MHC Class II expression were increased. In EAE, we observed an equivalent dampening of proinflammatory B-cell properties and an enhanced expression of MHC Class II. When used as antigen-presenting cells for activation of naive T cells, GA-treated B cells promoted development of regulatory T cells, whereas proinflammatory T-cell differentiation was diminished. Conclusions GA immune modulates B-cell function in EAE and MS and efficiently interferes with pathogenic B cell-T cell interaction.
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