Although glucocorticoids (GC) remain the corner stone of giant cell arteritis (GCA) treatment, GC-sparing strategies are needed because GC are responsible for side effects.1 Recent advances in the pathophysiology of GCA showed that CD4+ T cells are recruited in the arterial wall and polarised into Th1 and Th17 cells,2 3 the latter being sensitive to GC-mediated suppression, whereas Th1 response persists in GC-treated patients,2 which triggers the recruitment of macrophages4 and could be implicated in the occurrence of relapses when GC are tapered. Interleukin (IL)-12 and IL-23 are two cytokines involved in Th1 and Th17 polarisations, respectively.5 These two cytokines share a common subunit (p40), which allows ustekinumab, a humanised anti-p40 monoclonal antibody, to target both IL-12 and IL-23 pathways, thus disrupting in theory Th1 and Th17 immune responses.6 Recently, an open-label study reported on the efficacy and safety of …

中文翻译：

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Ustekinumab 抑制巨细胞动脉炎患者的 Th1 和 Th17 极化

尽管糖皮质激素 (GC) 仍然是巨细胞动脉炎 (GCA) 治疗的基石，但仍需要保留 GC 的策略，因为 GC 会产生副作用。1 GCA 病理生理学的最新进展表明，CD4+ T 细胞在动脉中被募集壁并极化为 Th1 和 Th17 细胞，2 3 后者对 GC 介导的抑制敏感，而 Th1 反应在接受 GC 治疗的患者中持续存在，2 这会触发巨噬细胞的募集 4 并且可能与 GC 复发时发生复发有关锥。白细胞介素 (IL)-12 和 IL-23 是分别参与 Th1 和 Th17 极化的两种细胞因子。 5 这两种细胞因子共享一个共同的亚基 (p40)，这使得优特克单抗（一种人源化抗 p40 单克隆抗体）能够靶向这两种 IL -12 和 IL-23 通路，