ArticleClinical and experimental medicine2015
Association of interleukin-10 promoter haplotypes with disease susceptibility and IL-10 levels in Mexican patients with systemic lupus erythematosus.
Article in Clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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10 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Association between complement 4 copy number variation and systemic lupus erythematosus: a meta-analysis.Clinical and experimental medicine · 2020Pooled it
- Study on the expression characteristics of CA125 in patients with SLE and its correlation with clinical indicators.Medicine · 2026Article
- Association of tumor necrosis factor α (rs1800629) and interleukin-10 (rs1800896) gene polymorphisms with systemic lupus erythematosus: a meta-analysis.Reumatologia · 2025Review
- The Impact of the IL-10 Gene Polymorphism on mRNA Expression and IL-10 Serum Concentration in Polish Lupus Patients.International journal of molecular sciences · 2024Article
- AlteredDiagnostics (Basel, Switzerland) · 2022Article
- IL10 haplotypes are associated with diabetic nephropathy susceptibility in patients from western Mexico.Journal of clinical laboratory analysis · 2019Article
- Association of interleukin 22 gene polymorphisms and serum IL-22 level with risk of systemic lupus erythematosus in a Chinese population.Clinical and experimental immunology · 2018Article
- The association between genetic variation in interleukin-10 gene and susceptibility to Henoch-Schönlein purpura in Chinese children.Clinical rheumatology · 2017Article
- Decreased UBASH3A mRNA Expression Levels in Peripheral Blood Mononuclear Cells from Patients with Systemic Lupus Erythematosus.Inflammation · 2015Article
- Interleukin-10 haplotypes are not associated with acute cerebral ischemia or high-risk transcranial Doppler in a newborn cohort of 395 children with sickle cell anemia.Revista brasileira de hematologia e hemoterapiaArticle
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10 authors at 2 institutions in 1 country.
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Abstract
Systemic lupus erythematosus (SLE) is the prototype autoimmune rheumatic disease. The etiology of this disease is incompletely understood; however, environmental factors and genetic predisposition are involved. Cytokine-mediated immunity plays a crucial role in the pathogenesis of SLE. We investigate the association of interleukin-10 (IL-10) promoter polymorphisms and their haplotypes in SLE patients from the western Mexico. One hundred and twenty-five SLE patients fulfilling the 1997 ACR criteria and 260 unrelated healthy subjects (HS), both Mexican mestizos, were genotyped for IL-10 -1082A>G, -819C>T, and -592C>A polymorphisms. Haplotypes were inferred using the expectation-maximization algorithm, then allele and haplotype distributions were compared between patients and HS, as well as patients with different clinical variables. We identified at -1082, -819, and -592 four predominant haplotypes ACC (43.70 % in patients vs 46.55 % in HS), ATA (21.45 vs 22.97 %), GCC (16.28 vs 14.21 %), and GTA (14.12 vs 14.12 %). The ATC haplotype was more frequent in SLE respect to HS, suggesting a risk effect (3.23 vs 1.05 %; OR 3.55, CI 1.14-11.11; p = 0.0293). SLE patient carriers of -592 CC genotype as well as the dominant model of inheritance showed higher sIL-10 respect to AA genotype, suggesting that -592 C allele is associated with increased production of the cytokine (p < 0.05). The ACC haplotype had higher IL-10 serum levels and higher values of Mexican version of the Systemic Lupus Erythematosus Disease Activity Index compared with the other haplotype carriers; however, no association was found regarding autoantibodies. Our data suggest that the IL-10 promoter haplotypes play an important role in the risk of developing SLE and influence the production of IL-10 in Mexican population. Nevertheless, further studies are required to analyze the expression of mRNA as well as to investigate the interacting epigenetic factors that could help to define the true contribution of this marker in SLE pathogenesis.
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