Gambelunghe G, Ghaderi M, Gharizadeh B, Brozzetti A, Tortoioli C, Del Sindaco P, Sanjeevi C B, Hjelmström P, Sirsjö A, Nyren P, Santeusanio F, Falorni A
Department of Internal Medicine, University of Perugia, Perugia, Italy.
Eur J Immunogenet. 2004 Apr;31(2):73-6. doi: 10.1111/j.1365-2370.2004.00447.x.
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.
白细胞向组织的趋化作用对于炎症和自身免疫反应的启动至关重要。这一过程由趋化因子控制，趋化因子是一类趋化性细胞因子。我们研究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的易感性相关。采用焦磷酸测序法对CCR2-64I进行基因分型，采用聚合酶链反应和凝胶检测法对CCR5-Delta32进行基因分型，对56例患者和127例健康对照进行了检测。未发现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病遗传风险和/或提供保护方面不起主要作用。
