Changing concepts in pathophysiology of the vasculitides

C. R. Robertson, R. M. McCallum

Research output: Contribution to journalArticle

11 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)3-10
Number of pages8
JournalCurrent Opinion in Rheumatology
Volume6
Issue number1
StatePublished - 1994
Externally publishedYes

Fingerprint

Vasculitis
Antineutrophil Cytoplasmic Antibodies
Cytokines
Humoral Immunity
Antigen-Antibody Complex
Cellular Immunity
Blood Vessels
Necrosis
Up-Regulation
Endothelial Cells
Inflammation
T-Lymphocytes
Infection
Pharmaceutical Preparations
Neoplasms
Proteins

ASJC Scopus subject areas

  • Immunology
  • Rheumatology

Cite this

Changing concepts in pathophysiology of the vasculitides. / Robertson, C. R.; McCallum, R. M.

In: Current Opinion in Rheumatology, Vol. 6, No. 1, 1994, p. 3-10.

Research output: Contribution to journalArticle

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