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- W2792463397 abstract "Pathogenic autoantibodies to muscle-specific tyrosine kinase (MuSK) can be found in patients with myasthenia gravis (MG) who do not have detectable antibodies to the acetylcholine receptor. Although the autoantibody-mediated pathology is well understood, much remains to be learned about the cellular immunology that contributes to autoantibody production. To that end, our laboratory has investigated particular components associated with the cellular immunopathology of MuSK MG. First, we found that B cell tolerance defects contribute to the abnormal development of the naive repertoire, which indicates that dysregulation occurs before the production of autoantibodies. Second, both the naive and antigen-experienced memory B cell repertoire, which we examined through the application of high-throughput adaptive immune receptor repertoire sequencing, include abnormalities not found in healthy controls. This highlights a broad immune dysregulation. Third, using complementary approaches, including production of human monoclonal antibodies, we determined that circulating plasmablasts directly contribute to the production of MuSK-specific autoantibodies in patients experiencing relapse following B cell depletion therapy. These collective findings contribute to defining a mechanistic model that describes MuSK MG immunopathogenesis." @default.
- W2792463397 created "2018-03-29" @default.
- W2792463397 creator A5019387002 @default.
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- W2792463397 creator A5060170912 @default.
- W2792463397 creator A5069281297 @default.
- W2792463397 creator A5069816755 @default.
- W2792463397 date "2018-01-01" @default.
- W2792463397 modified "2023-10-13" @default.
- W2792463397 title "Mechanisms underlying B cell immune dysregulation and autoantibody production in MuSK myasthenia gravis" @default.
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- W2792463397 doi "https://doi.org/10.1111/nyas.13535" @default.
- W2792463397 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5793885" @default.
- W2792463397 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29381221" @default.