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- W2022237243 abstract "B cells are important effectors and regulators of adaptive and innate immune responses, inflammation and autoimmunity, for instance in anti-NMDA-receptor (NMDAR) encephalitis. Thus, pharmacological modulation of B-cell function could be an effective regimen in therapeutic strategies. Since the non-competitive NMDAR antagonist memantine is clinically applied to treat advanced Alzheimer`s disease and ketamine is supposed to improve the course of resistant depression, it is important to know how these drugs affect B-cell function. Non-competitive NMDAR antagonists impaired B-cell receptor (BCR)- and lipopolysaccharide (LPS)-induced B-cell proliferation, reduced B-cell migration towards the chemokines SDF-1α and CCL21 and downregulated IgM and IgG secretion. Mechanistically, these effects were mediated through a blockade of Kv1.3 and KCa3.1 potassium channels and resulted in an attenuated Ca2+-flux and activation of Erk1/2, Akt and NFATc1. Interestingly, NMDAR antagonist treatment increased the frequency of IL-10 producing B cells after BCR/CD40 stimulation. Non-competitive NMDAR antagonists attenuate BCR and Toll-like receptor 4 (TLR4) B-cell signaling and effector function and can foster IL-10 production. Consequently, NMDAR antagonists may be useful to target B cells in autoimmune diseases or pathological systemic inflammation. The drugs’ additional side effects on B cells should be considered in treatments of neuronal disorders with NMDAR antagonists." @default.
- W2022237243 created "2016-06-24" @default.
- W2022237243 creator A5012246833 @default.
- W2022237243 creator A5019684451 @default.
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- W2022237243 creator A5089460733 @default.
- W2022237243 creator A5090019954 @default.
- W2022237243 date "2014-12-01" @default.
- W2022237243 modified "2023-10-05" @default.
- W2022237243 title "NMDA-receptor antagonists block B-cell function but foster IL-10 production in BCR/CD40-activated B cells" @default.
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- W2022237243 doi "https://doi.org/10.1186/s12964-014-0075-5" @default.