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γ干扰素基因DNA甲基化水平与儿童乙型肝炎疫苗无/低免疫的关系

Relationship between DNA methylation level of interferon-γ gene and no/low immunity to hepatitis B vaccine in children
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摘要 目的探讨γ干扰素(IFN-γ)基因DNA甲基化水平与儿童乙型肝炎疫苗无/低免疫的关系。方法选取214名8~9月龄儿童,均完成0、1、6月乙型肝炎疫苗接种。根据HBsAb水平分为无/低应答组、正常/高应答组,比较两组IFN-γ基因10个CpG位点DNA甲基化水平,并分析其与乙型肝炎疫苗无/低免疫反应的关系。结果214例儿童中无应答6例、低应答81例、正常应答52例、高应答75例。无/低应答组IFN-γ基因44和93位点甲基化水平高于正常/高应答组(P<0.05)。Logistic回归分析显示,IFN-γ基因44位点[OR=1.320(1.031,1.934)]和93位点[OR=1.480(1.146,2.374)]高甲基化水平是儿童乙型肝炎疫苗无/低应答的危险因素(P<0.05)。结论IFN-γ基因44和93位点的DNA甲基化水平是儿童乙型肝炎疫苗无/低免疫反应的危险因素。 Aim To investigate the relationship between DNA methylation level of interferonγ(IFN-γ)gene and no/low immunity of hepatitis B vaccine in children.Methods A total of 214 children aged 8-9 months with hepatitis B vaccination completed in 0,1 and 6 months were selected.According to the level of HBsAb,they were divided into no/low response group and normal/high response group.The methylation levels of 10 CpG site of the IFN-γgene in the two groups were compared,and its association with no/low immune response to hepatitis B vaccine was analyzed.Results Of the 214 children,6 were non-responders,81 were low responders,52 were normal responders,and 75 were high responders.The methylation levels of IFN-γgene at sites of 44 and 93 in the non-/low-response group were higher than those in the normal/high-response group(P<0.05).Logistic regression analysis showed that the high hypermethylation levels of IFN-γgene at loci of 44[OR=1.320(1.031,1.934)]and 93[OR=1.480(1.146,2.374)]were child-related risk factors for no/low response to hepatitis B vaccine(P<0.05).Conclusion The DNA methylation levels of IFN-γgene at site of 44 and 93 are risk factors for no/low immune response to hepatitis B vaccine in children.
作者 蒙绪海 MENG Xuhai(Department of Pediatrics,Yangpu Economic Development Zone Hospital of Danzhou,Danzhou 570000,Hainan,China)
出处 《中南医学科学杂志》 CAS 2024年第3期477-479,共3页 Medical Science Journal of Central South China
关键词 γ干扰素基因 DNA甲基化 儿童 乙型肝炎 免疫应答 interferon-γgene DNA methylation children hepatitis B immune response
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