[Giant-cell arteritis pathogenesis].
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.
CHU de Dijon, service de médecine interne et immunologie clinique, 21000 Dijon, France.
Maxime
M
Samson
Bernard
B
Bonnotte
D000375:Aging / Q000276:immunology / Q000502:physiology; D013700:Giant Cell Arteritis / Q000175:diagnosis / Q000209:etiology* / Q000473:pathology / Q000628:therapy; D006801:Humans; D056724:Immunity, Humoral / Q000502:physiology; D015850:Interleukin-6 / Q000502:physiology; D008954:Models, Biological; D058990:Molecular Targeted Therapy
D015850:Interleukin-6