Delivery of an miR155 inhibitor by anti-CD20 single-chain antibody into B cells reduces the acetylcholine receptor-specific autoantibodies and ameliorates experimental autoimmune myasthenia gravis.
作者： Y.-Z. Wang , F.-F. Tian , M. Yan , J.-M. Zhang , Q. Liu
DOI: 10.1111/CEI.12265
关键词:
摘要: MicroRNA-155 (miR155) is required for antibody production after vaccination with attenuated Salmonella. miR155-deficient B cells generated reduced germinal centre responses and failed to produce high-affinity immunoglobulin (Ig)G1 antibodies. In this study, we observed up-regulation of miR155 in the peripheral blood mononuclear (PBMCs) patients myasthenia gravis (MG), was also up-regulated torpedo acetylcholine receptor (T-AChR)-stimulated cells. We used an inhibitor conjugated anti-CD20 single-chain treat both cultured experimental autoimmune MG (EAMG) mice. Our results demonstrated that silencing by its impaired cell-activating factor (BAFF)-R-related signalling pathway translocation nuclear (NF)-κB into nucleus. Additionally, AChR-specific autoantibodies were reduced, which may be related altered amounts marginal zone memory spleens EAMG study suggests a promising target clinical therapy MG.
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