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Previous Volume 349:160-169 July 10, 2003 Number 2 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Inflammation of large arteries such as the aorta and its major branches occurs in a number of disorders, including Kawasaki's syndrome, Behçet's syndrome, rheumatoid arthritis, syphilis, and tuberculosis. However, aortitis and large-vessel arteritis are characteristics of two entities — giant-cell (temporal) arteritis and Takayasu's arteritis. These arteritides involve similar histologic abnormalities¹ but differ in the age of onset and the vascular structures that are preferentially targeted.^2,3 They share pathogenic pathways that distinguish them from other vasculitides. Cellular immune responses involving T cells, antigen-presenting cells, and macrophages are fundamental elements in giant-cell arteritis and Takayasu's arteritis, and there is no evidence . . . [Full Text of this Article]

The Pathogenic Model of Giant-Cell Arteritis

T-Cell–Dependent Vasculitic Inflammation in Giant-Cell Arteritis

Vessel-Wall Inflammation

Granuloma Formation in Giant-Cell Arteritis

Mechanisms of Tissue Damage in Giant-Cell Arteritis

Response of Arteries to Immune-Mediated Injury

Heterogeneity of Clinical Disease and Its Pathogenic Correlates

Therapeutic Implications

Optimizing Corticosteroid Treatment

Combination Therapy

Aspirin

Source Information

From the Departments of Medicine and Immunology, Mayo Clinic, Rochester, Minn.

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