M. Samson, S. Audia, L. Martin, N. Janikashvili, B. Bonnotte
Service de Médecine Interne et Immunologie Clinique, CHU de Dijon, 2 Bd Mal de Lattre de Tassigny, 21000 Dijon, France. firstname.lastname@example.org
2013 Vol.31, N°1 ,Suppl.75 - PI 0065, PF 0073
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-γ 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-1β and IL-6, which are responsible for the general symptoms encountered in GCA.
PMID: 23663684 [PubMed]
Received: 28/01/2013 - Accepted : 19/02/2013 - In Press: 19/04/2013 - Published: 19/04/2013