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Yasumizu, Yoshiaki; Ohkura, Naganari; Murata, Hisashi; Kinoshita, Makoto; Funaki, Soichiro; Nojima, Satoshi; Kido, Kansuke; Kohara, Masaharu; Motooka, Daisuke; Okuzaki, Daisuke; Suganami, Shuji; Takeuchi, Eriko; Nakamura, Yamami; Takeshima, Yusuke; Arai, Masaya; Tada, Satoru; Okumura, Meinoshin; Morii, Eiichi; Shintani, Yasushi; Sakaguchi, Shimon; Okuno, Tatsusada; Mochizuki, Hideki
Nature communications, 07/2022, Letnik: 13, Številka: 1Journal Article
Abstract Myasthenia gravis (MG) is a neurological disease caused by autoantibodies against neuromuscular-associated proteins. While MG frequently develops in thymoma patients, the etiologic factors for MG are not well understood. Here, by constructing a comprehensive atlas of thymoma using bulk and single-cell RNA-sequencing, we identify ectopic expression of neuromuscular molecules in MG-type thymoma. These molecules are found within a distinct subpopulation of medullary thymic epithelial cells (mTECs), which we name neuromuscular mTECs (nmTECs). MG-thymoma also exhibits microenvironments dedicated to autoantibody production, including ectopic germinal center formation, T follicular helper cell accumulation, and type 2 conventional dendritic cell migration. Cell–cell interaction analysis also predicts the interaction between nmTECs and T/B cells via CXCL12 - CXCR4 . The enrichment of nmTECs presenting neuromuscular molecules within MG-thymoma is further confirmed immunohistochemically and by cellular composition estimation from the MG-thymoma transcriptome. Altogether, this study suggests that nmTECs have a significant function in MG pathogenesis via ectopic expression of neuromuscular molecules.
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in: SICRIS
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