ArticleArthritis and rheumatism2012
Increased frequency of complement C4B deficiency in rheumatoid arthritis.
Article in Arthritis and rheumatism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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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.
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Association of Fc Gamma Receptor 3B Gene Copy Number Variation with Rheumatoid Arthritis Susceptibility.Genes · 2022Pooled it
- The Intertwining Between Arthritis and Inborn Errors of Immunity.Journal of clinical medicine · 2026Review
- Distinct Effects of Complement C4A and C4B Copy Numbers in Systemic Sclerosis Serological and Clinical Subtypes.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Article
- Rheumatologic manifestations in children with underlying inborn errors of immunity.BMC rheumatology · 2025Article
- Human nasal turbinate stem cells with specific gene signatures (HAS2, CXCL1, KRTAP1-5, GSTT2B, and C4B) attenuate rheumatoid arthritis.Scientific reports · 2025Article
- The complement system and human autoimmune diseases.Journal of autoimmunity · 2023Review
- Genetics in Behcet's Disease: An Update Review.Frontiers in ophthalmology · 2022Review
- Human Complement C4B Allotypes and Deficiencies in Selected Cases With Autoimmune Diseases.Frontiers in immunology · 2021Article
- Association ofDisease markers · 2020Article
- Co-occurrence between C1 esterase inhibitor deficiency and autoimmune disease: a systematic literature review.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2020Article
- Article
- Association between C4, C4A, and C4B copy number variations and susceptibility to autoimmune diseases: a meta-analysis.Scientific reports · 2017Article
- Glycosylation patterns and PHA-E-associated glycoprotein profiling associated with early hepatic encephalopathy in Chinese hepatocellular carcinoma patients.American journal of translational research · 2016Article
- Early Components of the Complement Classical Activation Pathway in Human Systemic Autoimmune Diseases.Frontiers in immunology · 2016Review
- Primary complement and antibody deficiencies in autoimmune rheumatologic diseases with juvenile onset: a prospective study at two centers.Pediatric rheumatology online journal · 2015Observational
- Clinical implications of copy number variations in autoimmune disorders.The Korean journal of internal medicine · 2015Review
- Serum C-X-C motif chemokine 13 is elevated in early and established rheumatoid arthritis and correlates with rheumatoid factor levels.Arthritis research & therapy · 2014Article
- Pre-rheumatoid arthritis: predisposition and transition to clinical synovitis.Nature reviews. Rheumatology · 2012Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveTo assess the copy number variation of complement C4A and C4B genes in patients with rheumatoid arthritis (RA).
methodsDNA samples were obtained from 299 patients and controls and analyzed for copy number variation of total complement C4, C4A, and C4B genes. The results were compared by chi-square analysis, and odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated.
resultsChi-square analysis revealed similar distribution patterns of total C4 alleles in RA patients (n = 160), non-RA patients (n = 88), and healthy controls (n = 51). There was no trend toward C4A deficiency as in lupus. Significant differences in C4B distribution were observed in RA patients, in whom an ∼2-fold increase in the frequency of homozygous and/or heterozygous C4B deficiency (0 or 1 allele) (40%) was present relative to non-RA patients or healthy controls (both 21.6%). C4B deficiency was more frequent in seropositive RA patients than in seronegative RA patients (44% versus 31%). The odds of C4B deficiency were 2.99 (95% CI 1.58-5.65) (P = 0.0006) in seropositive RA patients relative to non-RA controls. These findings were confirmed in a larger healthy control cohort, yielding an OR of 1.83 (95% CI 1.21-2.76) (P = 0.0056). The association of the shared epitope with C4B deficiency was significantly greater in seropositive RA patients than in non-seropositive RA controls (96% versus 54.5%) (P < 0.0001), suggesting that C4B deficiency interacts with the shared epitope in the development of seropositive RA.
conclusionOur findings indicate a relationship between C4B copy number variation and RA that approximates that seen between C4A copy number variation and lupus. The concurrence of C4B deficiency and the shared epitope in seropositive RA may have broad implications for our understanding of RA pathogenesis.
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