doi: 10.1161/CIRCRESAHA.109.194266
© 2009 American Heart Association, Inc.
Editorials |
Giant Cell Arteritis
Dendritic Cells Take Two T’s to Tango
From the Clinic of Internal Medicine I (A.Y.), Department of Cardiology, University Hospital Jena, Germany; and Division of Pediatric Infectious Diseases and Immunology (M.A.), Burns and Allen Research Institute, Cedars-Sinai Medical Center and David Geffen School of Medicine at the University of California, Los Angeles.
Correspondence to Moshe Arditi, MD, Cedars Sinai Medical Center, Immunobiology Institute and Division of Pediatric Infectious Diseases and Immunology, Los Angeles, CA 90048. E-mail moshe.arditi@cshs.org
See related article, pages 488–495
Key Words: giant cell arteritis • inflammation • dendritic cells • Toll-like receptors
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Chronic inflammation in arteries takes many forms and the causes vary markedly. The most common form of arterial inflammation is atherosclerosis, where inflammation is generally limited to the neointima and sometimes the medial layer of medium and larger arteries. However, the deeper layers of arteries can also become inflamed as well. Giant cell arteritis (GCA) constitutes an example of chronic inflammation that may often affect all layers of the arterial wall, including the adventitia.1 The rapidly evolving concentric hyperplastic vascular lesions of GCA typically occur in large branches of the aorta, particularly the carotid and temporal arteries.1 Clinical features of GCA are generally the result of the downstream tissue ischemia caused by luminal obstruction and may be rather modest (eg, headaches) but can include blindness, jaw claudication, aneurysm, arterial rupture, stroke, and death.1 The diagnosis can be confirmed by biopsy, and diseased tissues exhibit a granulomatous panarteritis and the presence of giant cells (hence, the name).1 Inflammatory lesions in GCA consist of activated T cells, dendritic cells (DCs), and macrophages.2 The causes of GCA are not well understood, but as is the case with other forms of arterial inflammation, GCA appears to involve a breakdown of tolerance that seems to result from some interaction between host defenses and the arterial wall.3 Hence, GCA reflects features of autoimmune phenomena, as well as primary immune defects, but the details of both are unclear.
Recently, major advances have been made in understanding the pathogenesis of GCA, implicating adaptive immunity, particularly DCs, as an
Related Article:
Circ. Res. 2009 104: 488-495.