{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T02:49:30Z","timestamp":1778640570176,"version":"3.51.4"},"reference-count":23,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2022,9,27]],"date-time":"2022-09-27T00:00:00Z","timestamp":1664236800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:p>Myasthenia gravis (MG) is an autoimmune disease in which pathogenic immunoglobulin\u2009G antibodies bind to acetylcholine receptors (or to functionally related molecules at the neuromuscular junction). B cell expression of the inhibitory immunoglobulin\u2009G receptor, Fc\u2010gamma receptor (Fc\u03b3R)\u00a0IIB, maintains peripheral immune tolerance, and its absence renders B cells hyperresponsive to autoantigen. Here, we report that Fc\u03b3RIIB expression levels are substantially reduced in B lineage cells derived from immunotherapy\u2010na\u00efve patients with acetylcholine receptor antibody\u2010positive early\u2010onset MG. In contrast, genetic variants associated with impaired Fc\u03b3RIIB expression are not enriched in MG, indicating post\u2010transcriptional dysregulation. Fc\u03b3R\u2010targeted therapies could have therapeutic benefits in MG. 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