SynthesisAnnals of the rheumatic diseases2008
The MHC2TA -168A/G polymorphism and risk for rheumatoid arthritis: a meta-analysis of 6861 patients and 9270 controls reveals no evidence for association.
Synthesis in Annals of the rheumatic diseases, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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
14 citing papers in PubMed, 29 citations in OpenAlex.
- Class II Major Histocompatibility Complex Transactivator (CIITA): A Master MHC-II Regulator Impacting Cancer and Beyond.Journal of immunotherapy and precision oncology · 2026Review
- Chromosome structural variation analysis reveals lung cancer-associated gene regulatory networks in rheumatoid arthritis patients.BMC medical genomics · 2025Article
- Unraveling the nexus between lung cancer and rheumatoid arthritis using integrative transcriptomics and genomics.BMC cancer · 2025Article
- CIITA promoter polymorphism impairs monocytes HLA-DR expression in patients with septic shock.iScience · 2022Article
- Effects of C2ta genetic polymorphisms on MHC class II expression and autoimmune diseases.Immunology · 2017Article
- MHC2TA and FCRL3 genes are not associated with rheumatoid arthritis in Mexican patients.Rheumatology international · 2016Article
- CIITA gene variants are associated with rheumatoid arthritis in Scandinavian populations.Genes and immunity · 2012Article
- Article
- The rs4774 CIITA missense variant is associated with risk of systemic lupus erythematosus.Genes and immunity · 2011Article
- CIITA is not associated with risk of developing rheumatoid arthritis.Genes and immunity · 2011Article
- Lack of association of the CIITA -168A→G promoter SNP with myasthenia gravis and its role in autoimmunity.BMC medical genetics · 2010Article
- CIITA variation in the presence of HLA-DRB1*1501 increases risk for multiple sclerosis.Human molecular genetics · 2010Article
- Regulation of major histocompatibility complex class II gene expression, genetic variation and disease.Genes and immunity · 2010Review
- The inextricable link between atherosclerosis and prototypical inflammatory diseases rheumatoid arthritis and systemic lupus erythematosus.Arthritis research & therapy · 2009Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAn association between major histocompatibility complex (MHC) genes, particularly those within the class II HLA region, and rheumatoid arthritis (RA) is well established, and accounts for an estimated 30% of the genetic component in RA. The MHC class II transactivator gene (MHC2TA) on chromosome 16p13 has recently emerged as the most important transcription factor regulating genes required for class II MHC-restricted antigen presentation. Previous studies of a promoter region polymorphism (-168A/G, rs3087456) in the MHC2TA gene and RA have yielded conflicting results.
objectiveTo assess the association of the MHC2TA -168A/G polymorphism (rs3087456) and risk for RA by meta-analysis.
methodsMeta-analysis was performed for 6861 patients with RA and 9270 controls from 10 case-control studies. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated for each study. Summary ORs and 95% CIs were calculated for random effects models.
resultsNo effect was observed for the G risk allele (OR 1.02, 95% CI 0.93 to 1.12, p = 0.70) or the GG risk genotype (OR 1.14, 95% CI 0.95 to 1.36, p = 0.16).
conclusionsOur results indicate that the MHC2TA -168A/G polymorphism (rs3087456) is not associated with RA yet underscore the importance of including shared epitope allele carrier status, secondary phenotypes and more complete characterisation of MHC2TA variation in future studies.
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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.