{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,12]],"date-time":"2026-04-12T09:17:02Z","timestamp":1775985422094,"version":"3.50.1"},"reference-count":28,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2012,1,12]],"date-time":"2012-01-12T00:00:00Z","timestamp":1326326400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2012,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:italic>Introduction<\/jats:italic>: HLA\u2010DQ8 transgenic mice develop ocular myasthenia gravis (oMG), which then progresses to generalized MG (gMG) when immunized with the human acetylcholine receptor (H\u2010AChR) \u03b1 subunit. Because the fetal AChR \u03b3 subunit is expressed in adult extraocular muscles, we anticipated that \u03b3 subunit immunization would generate an immune response to mouse AChR and induce MG in mice. <jats:italic>Results<\/jats:italic>: H\u2010AChR \u03b3 subunit immunization in HLA\u2010DQ8 mice induced an autoimmune response to mouse AChR and led to the destruction of AChR in the neuromuscular junction (NMJ) by anti\u2010AChR antibody and complement activation, and it triggered upregulation of AChR gene transcription. <jats:italic>Conclusion<\/jats:italic>: Our findings indicate that oMG may be induced by immunity to the AChR \u03b3 subunit. 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