Samson Maxime, Bonnotte Bernard
CHU de Dijon, service de médecine interne et immunologie clinique, 21000 Dijon, France.
Presse Med. 2012 Oct;41(10):937-47. doi: 10.1016/j.lpm.2012.07.005. Epub 2012 Aug 14.
Giant-cell arteritis (GCA) involves larges arteries, especially aorta and extra-cranial branches of external carotid. Histo-pathological lesions affect all the layers of the artery leading to a segmental and focal panarteritis with a polymorphic cell infiltrate including T cells, macrophages and multinucleated giant cells, a fragmented internal elastic lamina and an intimal hyperplasia. The pathophysiology of GCA is not fully understood. After dendritic cell activation in the adventitia, CD4T cells are recruited in the arterial wall and polarized into Th1 and Th17 cells that produce IFN-γ and IL-17. These cytokines activate macrophages, giant cells and smooth muscle cells inducing vascular remodeling leading to ischemic manifestations of GCA. Macrophages infiltrating the adventitia produce IL-1β and IL-6 that are responsible for general symptoms encountered in GCA. In this review, we discuss GCA pathogenesis, with emphasis on the role of IL-6 as a promising therapeutic target.
巨细胞动脉炎（GCA）累及大动脉，尤其是主动脉和颈外动脉的颅外分支。组织病理学病变累及动脉各层，导致节段性和局灶性全动脉炎，伴有多形性细胞浸润，包括T细胞、巨噬细胞和多核巨细胞，内弹力膜破碎和内膜增生。GCA的病理生理学尚未完全阐明。在外膜树突状细胞激活后，CD4 T细胞被募集到动脉壁并极化为产生IFN-γ和IL-17的Th1和Th17细胞。这些细胞因子激活巨噬细胞、巨细胞和平滑肌细胞，诱导血管重塑，导致GCA的缺血表现。浸润外膜的巨噬细胞产生IL-1β和IL-6，它们是GCA中出现的全身症状的原因。在本综述中，我们讨论GCA的发病机制，重点是IL-6作为一个有前景的治疗靶点的作用。
