New developments in the pathogenesis of systemic vasculitis

Curr Opin Rheumatol. 1996 Jan;8(1):1-11. doi: 10.1097/00002281-199601000-00001.


Over the past few years, novel pathogenic mechanisms leading to vascular inflammation and injury have been discovered. Circumstantial evidence that supports a pathogenic role for antineutrophil cytoplasmic antibodies (ANCA) in mediating vessel damage includes in vitro studies showing that ANCA promote neutrophil activation and endothelial injury. In addition, several animal models of ANCA-induced vasculitis and glomerulonephritis have been developed. The role of T cell-mediated immune mechanisms in vasculitis has been strengthened by molecular studies demonstrating clonal expansion of selected T cell populations in inflammatory foci, possibly recognizing a disease-relevant antigen. There is also increasing awareness of the important role that adhesion molecules may play in the development of vascular inflammatory infiltrates. The putative participation of cytokines and growth factors, released by inflammatory cells, in vessel occlusion and organ dysfunction, is a focus of increasing research activity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antibodies, Antineutrophil Cytoplasmic / blood
  • Cell Adhesion Molecules / immunology
  • Cytokines / immunology
  • Growth Substances / immunology
  • Humans
  • Myeloblastin
  • Neutrophils / immunology
  • Peroxidase / immunology
  • Serine Endopeptidases / immunology
  • T-Lymphocytes / immunology
  • Vasculitis / blood*


  • Antibodies, Antineutrophil Cytoplasmic
  • Cell Adhesion Molecules
  • Cytokines
  • Growth Substances
  • Peroxidase
  • Serine Endopeptidases
  • Myeloblastin