ArticleScientific reports2017
Increased Complement 3a Receptor is Associated with Behcet's disease and Vogt-Koyanagi-Harada disease.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- The evolving landscape of complement therapeutics in rheumatology.Annals of the rheumatic diseases · 2026Review
- Single-cell RNA sequencing of intestinal Behçet's disease identifies putative pathogenic programs and potential therapeutic targets.Biomolecules & biomedicine · 2026Article
- Macrophage expression of P2X7 controls autoimmune uveitis.Journal of neuroinflammation · 2025Article
- Plasma-Derived Small Extracellular Vesicles From VKH Patients Suppress T Cell Proliferation Via MicroRNA-410-3p Modulation of CXCL5 Axis.Investigative ophthalmology & visual science · 2023Article
- Beyond Systemic Lupus Erythematosus and Anti-Phospholipid Syndrome: The Relevance of Complement From Pathogenesis to Pregnancy Outcome in Other Systemic Rheumatologic Diseases.Frontiers in pharmacology · 2022Review
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- Comprehensive miRNA Analysis Using Serum From Patients With Noninfectious Uveitis.Investigative ophthalmology & visual science · 2020Article
- A case presentation of an IgA nephropathy patient with Vogt-Koyanagi-Harada syndrome.BMC nephrology · 2020Article
- Complement and local ocular inflammatory response: Chronic immune factors in myopia.Science progressReview
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Behcet's disease (BD) and Vogt-Koyanagi-Harada disease (VKH) are systemic and recurrent autoimmune diseases associated with abnormal T cell immune response. Complement 3a receptor (C3aR) and complement 5a receptor (C5aR) have been reported to be involved in T cell mediated autoimmune disease. This study aimed to investigate the role of C3aR and C5aR in these two diseases. The C3aR expression in PBMCs was increased in patients with active BD (aBD) and active VKH (aVKH). No statistical difference was found concerning the expression of C5aR in PBMCs between patients with aBD or aVKH and normal controls. After the intraocular inflammation in BD and VKH patients was controlled, the C3aR expression returned back to normal levels. The serum from patients with aBD and aVKH significantly induced C3aR expression by PBMCs. C3a induced IL-6, IL-1β and TNF-α secretion, while inhibited the production of IL-10 by monocytes. Activation of C3aR in CD4
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