ArticleClinical and experimental immunology1999
Anti-proteinase-3 (PR3) antibodies (C-ANCA) recognize various targets on the human umbilical vein endothelial cell (HUVEC) membrane.
Article in Clinical and experimental immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Identification of Renal Transcripts Associated with Kidney Function and Prognosis in ANCA-Associated Vasculitis.Journal of the American Society of Nephrology : JASN · 2026Article
- Cerebrovascular involvement in systemic childhood vasculitides.Clinical rheumatology · 2023Review
- Mechanisms of thrombosis in ANCA-associated vasculitis.Clinical rheumatology · 2021Review
- Endothelial dysfunction in patients with granulomatosis with polyangiitis: a case-control study.Rheumatology international · 2018Article
- Myocardial ischemia in Wegener's granulomatosis: coronary atherosclerosis versus vasculitis.The open cardiovascular medicine journal · 2010Article
- Polyarteritis nodosa and microscopic polyangiitis: etiologic and diagnostic considerations.Current rheumatology reports · 2002Review
- Role of proteinase 3 in activation of endothelium.Springer seminars in immunopathology · 2001Review
Corrections and comments
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Authors and funding
5 authors.
Funding
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Abstract
Numerous studies suggest that C-ANCA are directly pathogenic in vasculitis by activating leucocytes (oxidative burst, enzyme release, endothelial cytotoxicity, etc.). We and others have shown that C-ANCA can also directly activate HUVEC, but the precise target on HUVEC is unknown. We show in this study that C-ANCA recognize various targets on the HUVEC membrane (different from PR3 in our model), leading to secondary cell activation. Polyclonal affinity-purified C-ANCA recognized targets on the unfixed endothelial membrane in fluorescent ELISA, flow cytometry, and immunoprecipitation studies. C-ANCA did not react with Fcgamma receptors. Reverse transcriptase-polymerase chain reaction (RT-PCR) experiments showed that HUVEC did not express PR3. The targets of polyclonal and monoclonal anti-PR3 antibodies on the endothelial membrane were not the same. Some epitopes were lost after trypsin-EDTA digestion and formaldehyde fixation of cells, whereas anti-PR3 targeted unfixed HUVEC. This suggests that anti-PR3 react with the endothelial membrane and recognize conformational epitopes shared with PR3. Endothelial cells may thus participate in the inflammation associated with Wegener's granulomatosis and contribute to the emergence of clinical manifestations.
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