ArticleClinical and experimental immunology2001
Increased expression of CTLA-4 (CD152) by T and B lymphocytes in Wegener's granulomatosis.
Article in Clinical and experimental immunology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 78 citations in OpenAlex.
- Immune checkpoint imbalance in ANCA-associated vasculitis: insights into disease activity and precision immunotherapy.Frontiers in medicine · 2026Review
- ANCA-associated vasculitis with crescentic glomerulonephritis and papillary thyroid carcinoma: A case report.Medicine · 2025Article
- ANCA-associated vasculitis and lung cancer: an immunological perspective.Clinical and experimental medicine · 2024Review
- Catecholamines' accumulation and their disturbed metabolism at perilesional site: a possible cause of vitiligo progression.Archives of dermatological research · 2023Article
- Targeting immune checkpoints in anti-neutrophil cytoplasmic antibodies associated vasculitis: the potential therapeutic targets in the future.Frontiers in immunology · 2023Review
- Antineutrophil Cytoplasmic Antibody-Associated Vasculitis Update: Genetic Pathogenesis.Frontiers in immunology · 2021Review
- Categorisation of patients based on immune profiles: a new approach to identifying candidates for response to checkpoint inhibitors.Clinical & translational immunology · 2021Article
- Unraveling the Immunopathogenesis and Genetic Variants in Vasculitis Toward Development of Personalized Medicine.Frontiers in cardiovascular medicine · 2021Review
- Immune Checkpoints, a Novel Class of Therapeutic Targets for Autoimmune Diseases.Frontiers in immunology · 2021Review
- New Insights Into Novel Therapeutic Targets in ANCA-Associated Vasculitis.Frontiers in immunology · 2021Review
- T-lymphocyte in ANCA-associated vasculitis: what do we know? A pathophysiological and therapeutic approach.Clinical kidney journal · 2019Article
- The Co-inhibitor BTLA Is Functional in ANCA-Associated Vasculitis and Suppresses Th17 Cells.Frontiers in immunology · 2019Article
- CTLA-4 in mesothelioma patients: tissue expression, body fluid levels and possible relevance as a prognostic factor.Cancer immunology, immunotherapy : CII · 2016Article
- Dysregulation of peritoneal cavity B1a cells and murine primary biliary cholangitis.Oncotarget · 2016Article
- An open-label trial of abatacept (CTLA4-IG) in non-severe relapsing granulomatosis with polyangiitis (Wegener's).Annals of the rheumatic diseases · 2014Article
- Reply: To PMID 23553415.Arthritis and rheumatism · 2013Article
- The engagement of CTLA-4 on primary melanoma cell lines induces antibody-dependent cellular cytotoxicity and TNF-α production.Journal of translational medicine · 2013Article
- Pathogenesis of ANCA-associated vasculitis.Current rheumatology reports · 2012Review
- Clinical use of biologics in vasculitis syndromes.Biologics : targets & therapy · 2012Article
- Pathophysiological importance of antineutrophil antibodies in vasculitis.Current opinion in hematology · 2011Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CTLA-4 (CD152) is a surface molecule of activated T cells with sequence homology to CD28. Both molecules bind to the same ligands, B7.1 (CD80) and B7.2 (CD86) but have antagonistic functions. While CD28 is an important costimulator, CTLA-4 has an essential inhibitory function in maintaining the homeostasis of the immune system. Furthermore, CTLA-4 has a role in inducing a Th1 response and suppressing Th2 cytokines, an effect which is antagonized by CD28. Many autoimmune diseases are characterized by an overwhelming production of Th1 cytokines. Recently, the predominance of the Th1 cytokine pattern has been directly observed in the granulomatous inflammation of patients with Wegener's granulomatosis. The balance between CD28 and CTLA-4 expression by T lymphocytes could be a factor in the pathogenesis of autoimmune diseases. Down regulation of CD28 predominantly on CD8+ T cells has been described in Wegner's granulomatosis; however, analysis of CTLA-4 is complicated by its low expression levels. Here we have used potent signal enhancement to study CTLA-4 on PBMC in patients with Wegener's granulomatosis (n = 25) in comparison with healthy controls (n = 19). Expression levels of CTLA-4 were significantly increased selectively on CD4+ and possibly also on CD4-/CD8- T cells in Wegener's granulomatosis. High CTLA-4 expression by T lymphocytes was associated with more severe disease. In contrast, after stimulation with the mitogen PHA, CTLA-4 levels were strongly increased on T cells from controls but in T cells from Wegener's granulomatosis patients this response was severely impaired. Interestingly, while CTLA-4 was seen exclusively on T cells in control individuals, about half of the Wegener's patients showed CTLA-4 expression by a fraction of peripheral B lymphocytes. CTLA-4 positive B cells in the periphery were associated with less acute disease.
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