alexa Giant-Cell Arteritis: Immunopathogenic Mechanisms Invol
ISSN: 2471-9544

Journal of Vasculitis
Open Access

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Review Article

Giant-Cell Arteritis: Immunopathogenic Mechanisms Involved in Vascular Inflammation and Remodeling

Ester Planas-Rigol, Marc Corbera-Bellalta, Georgina Espígol-Frigolé Nekane Terrades-García, Marco A Alba, Sergio Prieto-González, Hernández-Rodríguez, E Lozano and Maria C Cid*

Department of Autoimmune Diseases, Hospital Clínic, University of Barcelona, Spain

*Corresponding Author:
Maria C Cid
Department of Autoimmune Diseases
Hospital Clínic, University of Barcelona, Spain
Tel: +34 93 2279365
E-mail: [email protected]

Received date: December 21, 2015; Accepted date: January 18, 2016; Published date: January 24, 2016

Citation: Ester PR, Marc CB, Georgina EF, Marco AA, Sergio PG, et al. (2016) Giant-Cell Arteritis: Immunopathogenic Mechanisms Involved in Vascular Inflammation and Remodeling. J Vasc 2:103. doi: 10.4172/2471-9544.1000103

Copyright: © 2016 Rigol EP, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Giant-cell arteritis (GCA) is a large-vessel granulomatous vasculitis in which aging, gender and genetics likely play a significant role. The association with polymorphisms in the major histocompatibility complex suggests that GCA may be an antigen-driven disease. Immunopathology studies performed with temporal artery biopsies from patients with GCA have generated relevant clues regarding to pathogenesis by indicating participation of Th1 and Th17-mediated pathways, a prominent role for macrophages in tissue injury, and the relevance of vascular response to inflammation. Vascular wall elements, especially endothelial cells and vascular smooth muscle cells are not passive bystanders. Through expression of chemokines and adhesion molecules vascular cells contribute to the continuous recruitment of inflammatory cells that are able to enter the artery wall through newly formed neovessels. Inflammatory cell products, as well as vascular injury, trigger a vascular remodelling process. This eventually leads to the development of intimal hyperplasia and vascular lumen obliteration, source of ischemic complications.

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