Pathogenesis of giant cell arteritis: new insight into the implication of CD161+T cells.
Fiche publication
Date publication
janvier 2013
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BONNOTTE Bernard, Pr MARTIN Laurent
Tous les auteurs :
Samson M, Audia S, Martin L, Janikashvili N, Bonnotte B
Lien Pubmed
Résumé
Giant cell arteritis (GCA) is a granulomatous large-vessel vasculitis that usually affects the aorta and/or its major branches, especially the branches of the carotid arteries. Histo-pathological lesions are observed in all layers of the artery leading to segmental and focal panarteritis with a polymorphic cell infiltrate that includes T cells, macrophages and multinucleated giant cells, a fragmented internal elastic lamina and intimal hyperplasia. The pathophysiology of GCA is complex and not fully understood. In this review, we discuss the immunological aspects of GCA pathogenesis with a particular emphasis on T cell responses. Upon dendritic cell activation in the adventitia, CD4 T cells co-expressing CD161 are recruited in the arterial wall and polarised into Th1 and Th17 cells that produce IFN-gamma and IL-17, respectively. These cytokines activate macrophages, giant cells and vascular smooth muscle cells, thus inducing vascular remodelling which leads to the ischaemic manifestations of GCA. Macrophages infiltrating the adventitia produce IL-1 beta and IL-6, which are responsible for the general symptoms encountered in GCA.
Référence
Clin Exp Rheumatol. 2013 Jan-Feb;31(1 Suppl 75):S65-73