Changing concepts in pathophysiology of the vasculitides.
Vasculitis is a clinicopathologic process that involves inflammation and necrosis of blood vessels, resulting in a wide range of clinical diseases. The pathogenesis of vasculitis has been attributed to immunologic mechanisms, including immune complexes, cellular immunity, and humoral immunity, with numerous inciting events such as infection, drugs, malignancy, or toxins. Inflammatory cytokine production and adhesion molecule activation or upregulation are important determinants of the pathogenic inflammatory responses noted in vasculitis. Endothelial cells may be targeted by anti-endothelial cell antibodies and are central targets of numerous proinflammatory cytokines in vasculitis pathogenesis. Finally, antineutrophil cytoplasmic antibodies (ANCA) and T-cell responses to the protein targets of ANCA may play a role in vessel damage in ANCA-associated vasculitis.
Duke University Medical Center, Durham, North Carolina.
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CR
Robertson
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McCallum
D019268:Antibodies, Antineutrophil Cytoplasmic; D001323:Autoantibodies / Q000378:metabolism; D015551:Autoimmunity; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D002630:Chemotactic Factors / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis; D004730:Endothelium, Vascular / Q000503:physiopathology; D006413:Hematopoietic System / Q000503:physiopathology; D006801:Humans; D008247:Lysosomes / Q000201:enzymology; D008954:Models, Biological; D014657:Vasculitis / Q000209:etiology / Q000503:physiopathology*
D019268:Antibodies, Antineutrophil Cytoplasmic; D001323:Autoantibodies; D015815:Cell Adhesion Molecules; D002630:Chemotactic Factors; D016207:Cytokines