RT Journal Article
SR Electronic
T1 Glatiramer acetate immune modulates B-cell antigen presentation in treatment of MS
JF Neurology - Neuroimmunology Neuroinflammation
JO Neurol Neuroimmunol Neuroinflamm
FD Lippincott Williams & Wilkins
SP e698
DO 10.1212/NXI.0000000000000698
VO 7
IS 3
A1 Darius Häusler
A1 Zivar Hajiyeva
A1 Jan W. Traub
A1 Scott S. Zamvil
A1 Patrice H. Lalive
A1 Wolfgang Brück
A1 Martin S. Weber
YR 2020
UL http://nn.neurology.org/content/7/3/e698.abstract
AB 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-α 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.APC=antigen-presenting cell; EAE=experimental autoimmune encephalomyelitis; GA=glatiramer acetate; NMO=neuromyelitis optica; PBMC=peripheral blood mononuclear cell; PBS=phosphate-buffered saline; RRMS=relapsing-remitting MS; WT=wild type