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CDR3 Spectratyping Analysis of the TCR Repertoire in Myasthenia Gravis¹

Yoh Matsumoto^2,*, Hidenori Matsuo^,, Hiroshi Sakuma^*, Il-Kwon Park^*, Yukiko Tsukada^*, Kuniko Kohyama^*, Takayuki Kondo, Satoshi Kotorii and Noritoshi Shibuya^,

^* Department of Molecular Neuropathology, Tokyo Metropolitan Institute for Neuroscience, Fuchu, Tokyo, Japan; Division of Clinical Research and Department of Neurology, National Hospital Organization, Nagasaki Medical Center of Neurology, and Department of Clinical Neurosciences, Nagasaki University Graduate School of Biomedical Sciences, Kawatana, Nagasaki, Japan

Because myasthenia gravis (MG) is an autoimmune disease mediated by Abs specific for the acetylcholine receptor, helper T cells play a role in Ab production. In this study, we have performed large-scale cross-sectional and longitudinal TCR studies by CDR3 spectratyping using PBL and thymus tissues from MG patients. We found that there was no preferential usage of any particular TCR -chains that was identical among MG patients. However, the longitudinal study clearly demonstrated that one or more TCR V expansions persisted frequently in MG patients. Importantly, persistent TCR expansions correlated with clinical severity and high anti-acetylcholine receptor Ab titer. Finally, examinations of T cells expressing CXCR5, i.e., follicular B-helper T cells, revealed that spectratype expansions in MG patients were detected mainly in the CD4⁺ CXCR5⁺ T cell populations, whereas CD8⁺ T cells were the major source of clonal expansion in healthy subjects. These findings suggest that persistent clonal expansions of T cells in MG patients are associated with the development and maintenance of MG. Close examination of pathogenic T cells in MG provides useful information to elucidate the pathogenesis and to estimate the disease status.

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