Giant cell arteritis and Takayasu arteritis are autoimmune vasculitides that cause aneurysm formation and tissue infarction. Extravascular inflammation consists of an intense acute phase response. Deeper understanding of pathogenic events in the vessel wall has highlighted the loss of tissue protective mechanisms, the intrusion of immune cells into "forbidden territory", and the autonomy of self-renewing vasculitic infiltrates. Adventitial vasa vasora critically control vessel wall access and drive differentiation of tissue-invasive T cells. Selected T cells establish tissue residency and build autonomous, self-sufficient inflammatory lesions. Pathogenic effector T cells intrude and survive due to failed immune checkpoint inhibition. Vasculitis-sustaining T cells and macrophages provide a broad portfolio of effector functions, involving heterogeneous populations of pro-inflammatory T cells and diverse macrophage subsets that ultimately induce wall capillarization and intimal hyperplasia. Redirecting diagnostic and therapeutic strategies from control of extravascular inflammatory markers to suppression of vascular inflammation will improve disease management.

中文翻译：

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中型和大血管血管炎中的细胞因子、生长因子和蛋白酶。


巨细胞动脉炎和大动脉炎是导致动脉瘤形成和组织梗塞的自身免疫性血管炎。血管外炎症由强烈的急性期反应组成。对血管壁致病事件的更深入了解强调了组织保护机制的丧失、免疫细胞侵入“禁区”以及自我更新血管炎浸润的自主性。外膜血管至关重要地控制血管壁通路并驱动组织侵袭性 T 细胞的分化。选定的 T 细胞建立组织驻留并建立自主、自给自足的炎症病变。由于免疫检查点抑制失败，致病性效应 T 细胞入侵并存活。维持血管炎的 T 细胞和巨噬细胞提供广泛的效应功能，包括异质的促炎 T 细胞群和不同的巨噬细胞亚群，最终诱导血管壁毛细血管化和内膜增生。将诊断和治疗策略从控制血管外炎症标志物转向抑制血管炎症将改善疾病管理。