ArticleClinical and experimental immunology2005
Increased monocyte transcription of the proteinase 3 gene in small vessel vasculitis.
Article in Clinical and experimental immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- The evolving landscape of vasculitis management: past, current and emerging.Rheumatology (Oxford, England) · 2025Review
- A1AT dysregulation of metabolically stressed hepatocytes by Kupffer cells drives MASH and fibrosis.Experimental & molecular medicine · 2025Article
- Granulomatous Inflammation in ANCA-Associated Vasculitis.International journal of molecular sciences · 2021Review
- Pathogenesis and pathology of anti-neutrophil cytoplasmic antibody（ANCA）-associated vasculitis.Journal of translational autoimmunity · 2021Review
- ANCA autoantigen gene expression highlights neutrophil heterogeneity where expression in normal-density neutrophils correlates with ANCA-induced activation.Kidney international · 2020Article
- Innate immune cells in the pathogenesis of primary systemic vasculitis.Rheumatology international · 2016Review
- Histone modification signature at myeloperoxidase and proteinase 3 in patients with anti-neutrophil cytoplasmic autoantibody-associated vasculitis.Clinical epigenetics · 2016Article
- Neutrophil Extracellular Traps in ANCA-Associated Vasculitis.Frontiers in immunology · 2016Review
- Neutrophil-Related Gene Expression and Low-Density Granulocytes Associated With Disease Activity and Response to Treatment in Antineutrophil Cytoplasmic Antibody-Associated Vasculitis.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- Dysregulation of autoantigen genes in ANCA-associated vasculitis involves alternative transcripts and new protein synthesis.Journal of the American Society of Nephrology : JASN · 2015Article
- B cell-mediated pathogenesis of ANCA-mediated vasculitis.Seminars in immunopathology · 2014Review
- A myelopoiesis gene signature during remission in anti-neutrophil cytoplasm antibody-associated vasculitis does not predict relapses but seems to reflect ongoing prednisolone therapy.Clinical and experimental immunology · 2014Article
- Genetically determined severity of anti-myeloperoxidase glomerulonephritis.The American journal of pathology · 2013Article
- Phagocytosis of apoptotic cells by macrophages in anti-neutrophil cytoplasmic antibody-associated systemic vasculitis.Clinical and experimental immunology · 2012Article
- Neutrophil serine proteases promote IL-1β generation and injury in necrotizing crescentic glomerulonephritis.Journal of the American Society of Nephrology : JASN · 2012Article
- Elevated soluble Flt1 inhibits endothelial repair in PR3-ANCA-associated vasculitis.Journal of the American Society of Nephrology : JASN · 2012Article
- Impairment and Differential Expression of PR3 and MPO on Peripheral Myelomonocytic Cells with Endothelial Properties in Granulomatosis with Polyangiitis.International journal of nephrology · 2012Article
- Epigenetics and complementary proteins.Clinical and experimental immunology · 2011Review
- Epigenetic basis for aberrant upregulation of autoantigen genes in humans with ANCA vasculitis.The Journal of clinical investigation · 2010Article
- Elevated neutrophil membrane expression of proteinase 3 is dependent upon CD177 expression.Clinical and experimental immunology · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteinase 3 (PR3) is a pleiotropic and destructive serine protease and it is also a major target for autoantibodies in systemic small vessel vasculitis. We have shown recently that patients in stable remission have increased circulating levels of PR3, independent of autoantibody titre, inflammation, neutrophil degranulation and renal function. Here we explore the possibility of increased PR3 gene transcription. RNA was purified from peripheral blood monocytes from vasculitis patients and controls. Specific mRNA was measured by TaqMan real-time polymerase chain reaction (PCR). The monocyte-like cell lines THP-1 and U937 and human peripheral blod monocytes from healthy controls were stimulated with cytokines and lipopolysaccharide (LPS) for different time periods. PR3 protein was measured in plasma with enzyme-linked immunosorbent assay (ELISA). The median result for PR3 mRNA was 9.6 (1.8-680) for 22 patients, compared to 1 (0.1-2.8) for the 15 healthy controls. Elastase expression was also significantly increased, whereas myeloperoxidase and interleukin-8 were not. Stimulation of monocytes with tumour necrosis factor (TNF)-alpha, interferon (IFN)-gamma or LPS did not result in any increase of PR3 or elastase transcription, whereas interleukin (IL)-8 transcription was increased 10-fold. Circulating monocytes from patients with systemic vasculitis display increased PR3 gene transcription compared to healthy controls and patients with sytemic lupus erythematosus (SLE). This may be important for the development of vasculitis. Our results do not favour a role for cytokines, antineutrophil cytoplasmic antibodies (ANCA) or immunosuppressive medication in the upregulation of PR3 transcription in vasculitis.
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