| Title | Changing concepts in pathophysiology of the vasculitides. | | Author(s) | Robertson CR, McCallum RM | | Institution | Duke University Medical Center, Durham, North Carolina. | | Source | Curr Opin Rheumatol 1994 Jan; 6(1):3-10. | | MeSH | Antibodies, Antineutrophil Cytoplasmic
Autoantibodies
Autoimmunity
Cell Adhesion Molecules
Chemotactic Factors
Cytokines
Endothelium, Vascular
Hematopoietic System
Humans
Lysosomes
Models, Biological
Vasculitis
| | Abstract | 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. | | Language | eng | | Pub Type(s) | Journal Article
Review
| | PubMed ID | 8031677 |
|
