Abstract
NMDA-receptor antagonists block B-cell function but foster IL-10 production in BCR/CD40-activated B cells
Highlights
B cells are important effectors and regulators of adaptive and innate immune responses, inflammation and autoimmunity, for instance in anti-NMDA-receptor (NMDAR) encephalitis
B10 cells play a crucial role in preventing inflammatory and autoimmune pathologies [24,29,31,32] and a lack of or inhibition of B10 cells has been associated with exacerbated experimental autoimmune encephalitis (EAE) [33,34], collagen-induced arthritis [35] or colitis in mice [36]
NMDAR antagonists block B-cell proliferation induced by B-cell receptors (BCR) or LPS stimulation Splenic B cells were stimulated with anti-IgM (Fab’)2 fragment goat anti-mouse (α-IgM) to mimic BCR triggering by antigens, or with the Toll-like receptor 4 (TLR4) ligand LPS
Summary
B cells are important effectors and regulators of adaptive and innate immune responses, inflammation and autoimmunity, for instance in anti-NMDA-receptor (NMDAR) encephalitis. B cells are activated through the ligation of their antigen-specific B-cell receptors (BCR) and costimulatory ligands such as CD40, which drive their proliferation, survival and differentiation [1]. Systemic inflammation induced by LPS seems to affect neuronal pathology, for instance in multiple sclerosis, Alzheimer’s and Parkinson’s disease [7,8,9,10]. B cells can contribute to or induce diseases by production of auto-antibodies as in rheumatoid arthritis, lupus erythematosus and some neuronal disorders [7,37]. Pharmaceuticals that regulate B-cell function by modulating BCR- or TLR4-induced signaling are of interest as anti-inflammatory agents and immunotherapeutics [43,44]
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