SynthesisThe Journal of rheumatology2015
PTPN22 R620W polymorphism and ANCA disease risk in white populations: a metaanalysis.
Synthesis in The Journal of rheumatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Type I interferon production in myeloid cells is regulated by factors independent of Ptpn22.ImmunoHorizons · 2025Article
- Childhood-Onset ANCA-Associated Vasculitis: From Genetic Studies to Advances in Pathogenesis, Classification and Novel Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Review
- Genetic Polymorphism ofMedicina (Kaunas, Lithuania) · 2022Review
- Proautoimmune Allele of Tyrosine Phosphatase, PTPN22, Enhances Tumor Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Antineutrophil Cytoplasmic Antibody-Associated Vasculitis Update: Genetic Pathogenesis.Frontiers in immunology · 2021Review
- Modulation of TCR Signaling by Tyrosine Phosphatases: From Autoimmunity to Immunotherapy.Frontiers in cell and developmental biology · 2020Review
- The Contribution of PTPN22 to Rheumatic Disease.Arthritis & rheumatology (Hoboken, N.J.) · 2019Review
- Predictors of Poor Outcome in ANCA-Associated Vasculitis (AAV).Current rheumatology reports · 2016Review
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 3 countries.
Funding
Abstract
objectiveNo clear consensus has been reached on the PTPN22 R620W polymorphism and anti-neutrophil cytoplasmic antibody (ANCA) disease, especially when stratified by ANCA specificity and disease phenotypes.
methodsA metaanalysis was conducted on the PTPN22 R620W polymorphism across 4 studies in 1399 white patients with ANCA disease and 9934 normal control subjects.
resultsOverall, metaanalysis showed a statistically significant association between the A allele and ANCA disease in all subjects (OR 1.44, 95% CI 1.26-1.64, p < 0.00001), and stratification by disease category indicated the A allele was associated with granulomatosis with polyangiitis (Wegener's; GPA; OR 1.72, 95% CI 1.35-2.20, p < 0.0001) and microscopic polyangiitis (MPA; OR 1.53, 95% CI 1.08-2.15, p = 0.02) as compared to controls. However, when stratified by ANCA specificity, the association of the A allele was statistically evident among those with proteinase 3 (PR3) ANCA disease (OR 1.74, 95% CI 1.25-2.430, p = 0.001), with the same trend but not statistically associated with myeloperoxidase ANCA disease (OR 1.94, 95% CI 0.64-5.85, p = 0.24). The marked associations were also demonstrated between this allele with lung (OR 1.69, 95% CI 1.21-2.36, p = 0.002), ENT (OR 2.03, 95% CI 1.45-2.84, p < 0.0001), skin (OR 2.55, 95% CI 1.69-3.84, p < 0.0001), and peripheral neuropathy involvement (OR 2.12, 95% CI 1.39-3.22, p = 0.0005).
conclusionThe PTPN22 620W allele confers susceptibility to the occurrence and development of ANCA disease in whites, with specific evidence among subsets with GPA, MPA, and PR3 ANCA.
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