ArticleKidney international2008
ANCA patients have T cells responsive to complementary PR-3 antigen.
Article in Kidney international, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Friday Night Acute Kidney Injury: Chest Infection Masking Antineutrophil Cytoplasmic Antibody Vasculitis.Cureus · 2025Article
- The evolving landscape of vasculitis management: past, current and emerging.Rheumatology (Oxford, England) · 2025Review
- Childhood-Onset ANCA-Associated Vasculitis: From Genetic Studies to Advances in Pathogenesis, Classification and Novel Therapeutic Approaches.International journal of molecular sciences · 2024Review
- T-Cell Receptor Sequences Identify Combined Coxsackievirus-International journal of molecular sciences · 2024Article
- SARS-CoV-2 and Its Bacterial Co- or Super-Infections Synergize to Trigger COVID-19 Autoimmune Cardiopathies.International journal of molecular sciences · 2023Article
- Pathogenesis of anti-neutrophil cytoplasmic antibody-associated vasculitis.Rheumatology and immunology research · 2023Review
- T Cell Receptor Sequences Amplified during Severe COVID-19 and Multisystem Inflammatory Syndrome in Children Mimic SARS-CoV-2, Its Bacterial Co-Infections and Host Autoantigens.International journal of molecular sciences · 2023Article
- Toll-like Receptor 9 Induced Dendritic Cell Activation Promotes Anti-Myeloperoxidase Autoimmunity and Glomerulonephritis.International journal of molecular sciences · 2023Article
- Advances in the genomics of ANCA-associated vasculitis-a view from East Asia.Genes and immunity · 2021Review
- Human Proteinase 3, an important autoantigen of c-ANCA associated vasculitis, shares cross-reactive epitopes with serine protease allergens from mites: anF1000Research · 2021Article
- Pathogenesis and pathology of anti-neutrophil cytoplasmic antibody(ANCA)-associated vasculitis.Journal of translational autoimmunity · 2021Review
- ANCA-associated vasculitis.Nature reviews. Disease primers · 2020Review
- Pathogenesis of ANCA-Associated Pulmonary Vasculitis.Seminars in respiratory and critical care medicine · 2018Review
- Pathogenesis and treatment of ANCA-associated vasculitis-a role for complement.Pediatric nephrology (Berlin, Germany) · 2018Review
- Identification of Functional and Expression Polymorphisms Associated With Risk for Antineutrophil Cytoplasmic Autoantibody-Associated Vasculitis.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- ANCA-Associated Vasculitis Pathogenesis: A Commentary.Current rheumatology reports · 2017Review
- Overview of the Pathogenesis of ANCA-Associated Vasculitis.Kidney diseases (Basel, Switzerland) · 2016Review
- Autoimmunity to the alpha 3 chain of type IV collagen in glomerulonephritis is triggered by 'autoantigen complementarity'.Journal of autoimmunity · 2015Article
- Pathogenesis of antineutrophil cytoplasmic autoantibody-mediated disease.Nature reviews. Rheumatology · 2014Review
- B cell-mediated pathogenesis of ANCA-mediated vasculitis.Seminars in immunopathology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Some patients with proteinase 3 specific anti-neutrophil cytoplasmic autoantibodies (PR3-ANCA) also have antibodies that react to complementary-PR3 (cPR3), a protein encoded by the antisense RNA of the PR3 gene. To study whether patients with anti-cPR3 antibodies have cPR3-responsive memory T cells we selected conditions that allowed cultivation of memory cells but not naïve cells. About half of the patients were found to have CD4+TH1 memory cells responsive to the cPR3(138-169)-peptide; while only a third of the patients had HI-PR3 protein responsive T cells. A significant number of T cells from patients responded to cPR3(138-169) peptide and to HI-PR3 protein by proliferation and/or secretion of IFN-gamma, compared to healthy controls while there was no response to scrambled peptide. Cells responsive to cPR3(138-169)-peptide were not detected in MPO-ANCA patients suggesting that this response is specific. The HLADRB1(*) 15 allele was significantly overrepresented in our patient group and is predicted to bind cPR3(138-169) peptide with high affinity. Regression analysis showed a significant likelihood that anti-cPR3 antibodies and cPR3-specific T cells coexist in individuals, consistent with an immunological history of encounter with a PR3-complementary protein. We suggest that the presence of cells reacting to potential complementary protein pairs might provide an alternative mechanism for auto-immune diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.