Department of Dermatology and.
Department of Pathology, Columbia University, New York, New York, USA.
JCI Insight. 2018 Oct 4;3(19):121949. doi: 10.1172/jci.insight.121949.
Alopecia areata (AA) is an autoimmune disease in which cytotoxic T cells specifically target growing hair follicles. We used high-throughput TCR sequencing in the C3H/HeJ mouse model of AA and in human AA patients to gain insight into pathogenic T cell populations and their dynamics, which revealed clonal CD8+ T cell expansions in lesional skin. In the C3H/HeJ model, we observed interindividual sharing of TCRβ chain protein sequences, which strongly supports a model of antigenic drive in AA. The overlap between the lesional TCR repertoire and a population of CD8+NKG2D+ T cells in skin-draining lymph nodes identified this subset as pathogenic effectors. In AA patients, treatment with the oral JAK inhibitor tofacitinib resulted in a decrease in clonally expanded CD8+ T cells in the scalp but also revealed that many expanded lesional T cell clones do not completely disappear from either skin or blood during treatment with tofacitinib, which may explain in part the relapse of disease after stopping treatment.
斑秃(AA)是一种自身免疫性疾病,其中细胞毒性 T 细胞特异性靶向生长中的毛囊。我们使用 C3H/HeJ 小鼠 AA 模型和人类 AA 患者的高通量 TCR 测序,深入了解致病 T 细胞群体及其动态,这揭示了病变皮肤中克隆性 CD8+T 细胞的扩增。在 C3H/HeJ 模型中,我们观察到 TCRβ链蛋白序列的个体间共享,这强烈支持 AA 中的抗原驱动模型。病变 TCR 库与皮肤引流淋巴结中一群 CD8+NKG2D+T 细胞的重叠将该亚群鉴定为致病性效应物。在 AA 患者中,口服 JAK 抑制剂托法替尼治疗导致头皮中克隆性扩增的 CD8+T 细胞减少,但也表明在托法替尼治疗期间,许多扩增的病变 T 细胞克隆并没有完全从皮肤或血液中消失,这部分解释了治疗停止后疾病的复发。