中大弹性动脉的自体免疫血管炎可导致失明、中风、主动脉弓综合征和主动脉瘤。该疾病常常对免疫抑制治疗难以治愈，并在数十年内作为慢性主动脉炎持续进展。血管壁内肉芽肿性浸润的维持及组织浸润的T细胞和巨噬细胞是如何补充的尚不清楚。在血管炎动脉中，对免疫细胞群体的单细胞和全部组织转录组学研究鉴定出一种具有干细胞样特征的CD4+ T细胞群体。补给组织浸润和损伤效应T细胞的CD4+ T细胞在外膜微血管周围的第三类淋巴样结构中存活下来，在转录因子TCF1中表达，具有很高的增殖潜能，并产生EOMES+细胞毒性T细胞和BCL6+T滤泡辅助样细胞两个效应细胞群体。通过序列移植实验发现，表达白细胞介素7受体的TCF1hiCD4+ T细胞在维持血管炎方面发挥作用。因此，TCF1hiCD4+ T细胞发挥疾病干细胞的功能，促进自体免疫组织炎症的持久性和自主性。诱导缓解的治疗需以靶向CD4+ T细胞干细胞而非仅仅效应T细胞为前提。

Autoimmune vasculitis of the medium and large elastic arteries can cause blindness, stroke, aortic arch syndrome, and aortic aneurysm. The disease is often refractory to immunosuppressive therapy and progresses over decades as smoldering aortitis. How the granulomatous infiltrates in the vessel wall are maintained and how tissue-infiltrating T cells and macrophages are replenished are unknown. Single-cell and whole-tissue transcriptomic studies of immune cell populations in vasculitic arteries identified a CD4+ T cell population with stem cell-like features. CD4+ T cells supplying the tissue-infiltrating and tissue-damaging effector T cells survived in tertiary lymphoid structures around adventitial vasa vasora, expressed the transcription factor T cell factor 1 (TCF1), had high proliferative potential, and gave rise to two effector populations, Eomesodermin (EOMES)+ cytotoxic T cells and B cell lymphoma 6 (BCL6)+ T follicular helper-like cells. TCF1hiCD4+ T cells expressing the interleukin 7 receptor (IL-7R) sustained vasculitis in serial transplantation experiments. Thus, TCF1hiCD4+ T cells function as disease stem cells and promote chronicity and autonomy of autoimmune tissue inflammation. Remission-inducing therapies will require targeting stem-like CD4+ T cells instead of only effector T cells.