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首页> 外文期刊>European journal of immunogenetics: official journal of the British Society for Histocompatibility and Immunogenetics >Lack of association of human chemokine receptor gene polymorphisms CCR2-64I and CCR5-Delta32 with autoimmune Addison's disease.
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Lack of association of human chemokine receptor gene polymorphisms CCR2-64I and CCR5-Delta32 with autoimmune Addison's disease.

机译:人趋化因子受体基因多态性CCR2-64I和CCR5-Delta32与自身免疫性阿迪森氏病缺乏联系。

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Summary The attraction of leukocytes to tissues is essential for inflammation and the initiation of the autoimmune reaction. The process is controlled by chemokines, which are chemotactic cytokines. We investigated whether human chemokine receptor gene polymorphisms, namely CCR5-Delta32 and CCR2-64I, are associated with susceptibility to autoimmune Addison's disease. Genotyping was performed in 56 patients and 127 healthy controls by a new method using pyrosequencing for CCR2-64I and by polymerase chain reaction and detecting gel for CCR5-Delta32. None of the CCR2 or CCR5 alleles was found to be associated, either positively or negatively, with disease risk. Our results indicate that the CCR2-64I and CCR5-Delta32 gene polymorphisms do not play a major role in conferring genetic risk for, and/or protection against, autoimmune Addison's disease.
机译:总结白细胞对组织的吸引对于炎症和自身免疫反应的启动是必不可少的。该过程由趋化因子(趋化性细胞因子)控制。我们调查了人类趋化因子受体基因多态性,即CCR5-Delta32和CCR2-64I,是否与自身免疫性艾迪生病易感性相关。通过使用焦磷酸测序对CCR2-64I进行测序,聚合酶链反应和对CCR5-Delta32进行凝胶检测的新方法,对56例患者和127名健康对照进行基因分型。没有发现CCR2或CCR5等位基因与疾病风险呈正相关或负相关。我们的结果表明,CCR2-64I和CCR5-Delta32基因多态性在赋予自身免疫性艾迪生氏病遗传风险和/或预防自身免疫性方面没有发挥主要作用。

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