Leukocyte-endothelial interactions in antineutrophil cytoplasmic antibody-associated systemic vasculitis

Lorraine Harper, Caroline Savage

Research output: Contribution to journalReview article

12 Citations (Scopus)


The etiology of ANCA-associated vasculitis is unknown. Currently, it is believed that disease may be triggered by infection with the release of proinflammatory cytokines in genetically susceptible individuals. Priming of PMNs and endothelial cells by these cytokines allows ANCAs to activate PMNs, with damage localized to the endothelium, resulting in early lesions. Damage and activation of endothelial cells produces proinflammatory chemokines and cytokines with influxes of monocytes and T cells that intensify endothelial damage. In the kidney, these changes eventually lead to crescent formation. Antigen-specific memory T cells persist after disease remission with the potential of reactivation and disease relapse. Although our understanding of the pathophysiologic mechanisms of ANCA-associated vasculitis is far greater now than when ANCAs were first identified in 1982, more experimental work in combination with clinical observations is required to further elucidate these mechanisms.
Original languageEnglish
Pages (from-to)887-903
Number of pages17
JournalRheumatic Diseases Clinics of North America
Publication statusPublished - 1 Jan 2002


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