Giant-Cell Arteritis: Immunopathogenic Mechanisms Involved in Vascular Inflammation and Remodeling
Received Date: Dec 21, 2015 / Accepted Date: Jan 18, 2016 / Published Date: Jan 24, 2016
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.
Keywords: Vasculitis; Giant-cell arteritis; Genetic polymorphisms; Inflammation; Cytokines; Growth factors; Angiogenesis; Vascular remodelling
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: 10.4172/2471-9544.100103
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.
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