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IL-10 Promoter Polymorphisms (il-10 + promoter_polymorphism)
Selected AbstractsThe combinations of TNF,,308 and IL-6 ,174 or IL-10 ,1082 genes polymorphisms suggest an association with susceptibility to sporadic late-onset Alzheimer's diseaseACTA NEUROLOGICA SCANDINAVICA, Issue 6 2009P. Vural Objective,,, Single nucleotide polymorphisms in the regulatory regions of the cytokine genes for tumor necrosis factor , (TNF,), interleukin (IL)-6 and IL-10 have been suggested to influence the risk of Alzheimer's disease (AD) with conflicting results. Aim,,, To investigate the TNF,,308, IL-6 ,174 and IL-10 ,1082 gene polymorphisms as susceptibility factors for AD. Methods,,, We analyzed genotype and allele distributions of these polymorphisms in 101 sporadic AD patients and 138 healthy controls. Results,,, Heterozygotes (AG) or combined genotype (AG+AA) for IL-10 ,1082 were associated with approximately two-fold increase in the risk of AD. Carriers of A alleles of both TNF,,308 and IL-10 ,1082 had 6.5 times higher risk for AD in comparison with non-carriers. Concomitant presence of both mutant TNF,,308 A and IL-6 ,174 C alleles raised three-fold the AD risk, whereas there was no notable risk for AD afflicted by IL-6 ,174 polymorphism alone. Conclusion,,, Our results suggest that TNF, and IL-10 promoter polymorphism might be a risk factor for AD. The combined effects of TNF,,308, IL-6 ,174 and IL-10 ,1082 variant alleles may be more decisive to induce functional differences and modify the risk for AD. [source] IL-10 promoter haplotype influence on interferon treatment response in multiple sclerosisEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2005S. Wergeland The level of interleukin-10 (IL-10) expression is related to polymorphisms -1082 (G/A), -819 (T/C) and -592 (A/C) in the promoter region of the IL-10 gene, which constitute three haplotypes, GCC, ATA, and ACC. The ATA (a non-GCC) haplotype, which is associated with low IL-10 expression, has been shown to improve interferon (IFN) treatment response in hepatitis C. We analysed the distribution of IL-10 promoter haplotype combinations to determine whether they could influence initial IFN treatment response in 63 patients with relapsing-remitting multiple sclerosis (MS). The patients were grouped into non-GCC or GCC haplotypes, and the clinical and magnetic resonance imaging (MRI) disease activity was compared in the two groups. During the first 6 months of treatment, MS patients with non-GCC haplotypes experienced fewer new MRI T1-contrast enhancing lesions [0.77 ± 0.36 (SEM)] than patients with the GCC haplotype (2.45 ± 0.57) (P = 0.05, Mann-Whitney U test). No differences were detected on clinical disease activity. The results suggest an influence of IL-10 promoter polymorphisms on IFN treatment response in MS. [source] Interleukin-10 gene promoter polymorphism in Polish rheumatoid arthritis patientsINTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 4 2010A. Paradowska-Gorycka Summary Interleukin (IL)-10 is an important multifunctional cytokine with both anti-inflammatory and immunoregulatory effects in rheumatoid arthritis (RA). In the present study, we evaluated the frequency and potential impact of IL-10 promoter polymorphisms on susceptibility to and severity of RA in Polish in , patients with a high disease activity (mean DAS 28 C-reactive protein 5.25). DNA was obtained from 244 RA patients and 106 healthy controls. The ,592C/A and ,1082G/A IL-10 gene polymorphisms were amplified by polymerase chain reaction with restriction endonuclease mapping. The frequency of the IL-10-592CA, -592AA genotypes (respectively: 30% vs 5% and 7% vs 0%) and allele ,592A (37% vs 5%) were significantly higher in RA patients as compared with a control group. We did not find any association of the IL-10-592C/A genotype distribution with disease parameters, except for an increased ESR (erythrocyte sedimentation rate) in patients with the ,592CC genotype as compared with those with ,592CA or ,592AA genotypes (P = 0.01). The frequency of the IL-10-1082GG genotype was lower (P = 0.0001), and that of the IL-10-1082GA genotype was higher (P = 0.009) in RA patients comparing with the control group. In RA patients with ,1082GA or ,1082AA genotypes the time duration of the disease (P = 0.03), Health Assessment Questionnaire (HAQ) Score (P = 0.04) and PLT count (P = 0.001) were significantly increased as compared with subjects with ,1082GG genotype. Presented findings indicate that IL-10-592C/A and IL-10-1082G/A polymorphisms may be considered genetic risk factors for RA susceptibility and severity. [source] Single nucleotide polymorphisms in the interferon-, and interleukin-10 genes do not influence chronic hepatitis C severity or T-cell reactivity to hepatitis C virusLIVER INTERNATIONAL, Issue 2 2004William G.H. Abbott Abstract: Background: The mechanisms by which interferon-, (IFN-,) contributes to inter-individual heterogeneity in the severity of chronic hepatitis C (CH-C) are unknown. In 116 consecutive patients with CH-C, we tested the hypothesis that host genetic factors regulating IFN-, production and activity influence the severity of liver damage and hepatitis C virus (HCV)-specific T-cell reactivity. Methods: We determined the genotypes of functionally significant polymorphisms in the IFN-, gene and in the promoter of interleukin-10 (IL-10), a cytokine that counteracts IFN-,. We also measured concanavalin A (Con A)-stimulated IL-10 and IFN-, production, and the frequency of virus-specific T-cells, producing IFN-, or IL-10. Results: The grade of inflammation and the stage of fibrosis of CH-C showed no associations with either the IFN-, or IL-10 promoter polymorphisms or with Con A-stimulated IL-10 or IFN-, production. Similarly, there were no associations between HCV-specific T-cell frequencies and these host genetic factors. On multivariate analysis, the grade of inflammation and the duration of HCV infection accounted for only 37% of the variance in the stage of CH-C (P<0.0001). This percentage did not increase by including any genetic variables in the analyses. Conclusion: Future studies investigating the entire cytokine gene sequences will provide better information regarding genetic variations responsible for inter-individual differences in the severity of CH-C. [source] Combined effect of IL-10 and TGF-,1 promoter polymorphisms as a risk factor for aspirin-intolerant asthma and rhinosinusitisALLERGY, Issue 8 2009S.-H. Kim Background:, It has been known that interleukin (IL)-10 promoter polymorphisms at ,1082A/G, ,819T/C and ,592A/C, may influence IL-10 expression and associate with asthma. Interleukin-10 facilitates the regulatory function of transforming growth factor (TGF)-,. The goal of this study was to investigate a gene,gene interaction between IL-10 and TGF-,1 polymorphisms in Korean asthmatics with aspirin hypersensitivity. Methods:, Single-nucleotide polymorphism genotyping of IL-10 and TGF-,1 genes was performed and the functional effect of the IL-10 polymorphisms was analysed applying a luciferase reporter assay and an electrophoretic mobility shift assay. Results:, Among the patients with asthma, polymorphism at ,1082A/G was significantly associated with the phenotype of aspirin-intolerant asthma, AIA (P = 0.007, Pc = 0.021). Moreover, a synergistic effect between the TGF-,1,509C/T and IL-10,1082A/G polymorphisms on the phenotype of AIA was noted; when stratified by the presence of rhinosinusitis, the frequency of rare alleles (the CT or TT genotype of TGF-,1,509C/T and AG or GG genotype of IL-10,1082A/G) was significantly higher in the patients with AIA (15.2%) when compared with those with ATA (6.3%, P = 0.031; odds ratio 4.111; 95% confidence interval 1.504,11.235). In an in vitro functional assay, the ,1082G reporter plasmid exhibited significantly greater promoter activity when compared with the ,1082A construct in Jurkat T cells (P = 0.011). Moreover, we found that the transcription factor Myc-associated zinc-finger protein preferentially bound the ,1082G allele. Conclusion:, Our results suggest that IL-10 promoter polymorphisms contribute to the development of AIA and that rhinosinusitis may interact genetically with TGF-,1. [source] | ||||||||||