Sakuma Hiroshi, Katayama Ayako, Saito Yoshiaki, Komaki Hirofumi, Nakagawa Eiji, Sugai Kenji, Sasaki Masayuki
Department of Child Neurology, National Center of Neurology and Psychiatry, Tokyo, Japan.
Brain Dev. 2011 May;33(5):442-4. doi: 10.1016/j.braindev.2010.08.002. Epub 2010 Aug 24.
Dysfunction of CD4(+)CD25(+) regulatory T cell (Treg) has been demonstrated to play an important role in the development of autoimmune myasthenia gravis. This T cell subset, which has potent regulatory properties against immune response, has been reported to have a numerical or functional defect in patients with myasthenia gravis. We examined various T cell subsets, including CD4(+)CD25(+)Treg in peripheral blood mononuclear cells using flow cytometry in a pediatric patient suffering from ocular myasthenia gravis. Contrary to previous reports, the percentage of CD4(+)CD25(+)Treg in peripheral blood decreased significantly after successful treatment with prednisolone. This discrepancy could result from diversity within the immunopathogenesis of myasthenia gravis and may underpin a particular subgroup of myasthenia gravis seen in the East-Asian pediatric population.
CD4(+)CD25(+)调节性T细胞（Treg）功能障碍已被证明在自身免疫性重症肌无力的发病中起重要作用。据报道，这个对免疫反应具有强大调节特性的T细胞亚群在重症肌无力患者中存在数量或功能缺陷。我们使用流式细胞术检测了一名患有眼肌型重症肌无力的儿科患者外周血单个核细胞中的各种T细胞亚群，包括CD4(+)CD25(+)Treg。与之前的报道相反，泼尼松龙成功治疗后外周血中CD4(+)CD25(+)Treg的百分比显著下降。这种差异可能源于重症肌无力免疫发病机制的多样性，并可能是东亚儿科人群中所见的特定重症肌无力亚组的基础。
