SynthesisZeitschrift fur Rheumatologie2015
Meta-analysis of the association between functional MICA-TM polymorphisms and systemic lupus erythematosus, rheumatoid arthritis and ankylosing spondylitis.
Synthesis in Zeitschrift fur Rheumatologie, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- MICA and NLRP3 gene polymorphisms interact synergistically affecting the risk of ankylosing spondylitis.Immunologic research · 2024Article
- Relationship between rs4349859 and rs116488202 polymorphisms close to MHC-I region and serum urate levels in patients with gout.Molecular biology reports · 2023Article
- Increased Concentrations of Circulating Soluble MHC Class I-Related Chain A (sMICA) and sMICB and Modulation of Plasma Membrane MICA Expression: Potential Mechanisms and Correlation With Natural Killer Cell Activity in Systemic Lupus Erythematosus.Frontiers in immunology · 2021Article
- Constraints on Biological Mechanism from Disease Comorbidity Using Electronic Medical Records and Database of Genetic Variants.PLoS computational biology · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe aim of this study was to determine whether the major histocompatibility complex class I chain-related gene A transmembrane (MICA-TM) polymorphism is associated with susceptibility to systemic lupus erythematous (SLE), rheumatoid arthritis (RA) and ankylosing spondylitis (AS).
methodsA meta-analysis was conducted to establish the association between MICA-TM polymorphisms and SLE, RA and AS in the overall study population, as well as in each ethnic group.
resultsA total of 13 comparison studies, including five SLE (1601 patients; 1846 controls), four RA (701 patients; 887 controls) and four AS (346 patients; 356 controls) studies were considered in the meta-analysis. An association between the MICA-TM A5.1 allele and SLE was demonstrated in Europeans but not in Asians: odds ratio (OR) = 1.699, 95 % confidence interval (CI) = 1.123-2.569, p = 0.012 and OR = 0.949, 95 % CI = 0.502-1.793, p = 0.871, respectively. However, no association was found in Europeans after Bonferroni correction (pcorrected = 0.060). An association was found between the MICA-TM A9 allele and RA in Asians (OR = 0.527, 95 % CI = 0.408-0.681, p = 8.9 × 10(-7)) but not in Europeans; the association in Asians remained significant after Bonferroni correction (pcorrected = 4.5 × 10(-6)). An association between the MICA-TM A4 phenotype and AS was observed in European and Asian populations (OR = 12.87, 95 % CI = 6.747-24.58, p < 1.0 × 10(-9) and OR = 9.461, 95 % CI = 5.754-15.55, p < 1.0 × 10(-9), respectively). Meta-analysis stratified by human leukocyte antigen (HLA)-B27 status revealed an association between the MICA-TM A4 phenotype and HLA-B27 positivity AS in Asians, but not in Europeans (OR = 0.318, 95 % CI = 0.102-0.995, p = 0.049 and OR = 2.080, 95 % CI = 0.422-10.25, p = 0.368, respectively). However, the association in Asians was not significant after Bonferroni correction (pcorrected = 0.245).
conclusionThis meta-analysis demonstrated that there was no association between MICA-TM polymorphisms and SLE susceptibility, but that the MICA-TM A9 allele was associated with an RA risk in Asians. Moreover, the association between the MICA-TM A4 phenotype and AS was HLA-B27-dependent.
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