Hussein Y M, Ahmad A S, Ibrahem M M, El Tarhouny S A, Shalaby S M, Elshal A S, El Said M
Medical Biochemistry Department, Faculty of Medicine, Zagazig University, Egypt.
J Investig Allergol Clin Immunol. 2009;19(4):292-8.
The aim of this study was to clarify the role of interferon (IFN) gamma in the diagnosis and follow-up of atopic patients. We genotyped the IFN-gamma polymorphism at position +874 to examine the relationship between serum levels of IFN-gamma and disease severity and the role of IFN-gamma as a biochemical and immunologic marker.
The study population comprised 75 patients suffering from atopic asthma, atopic dermatitis, and allergic rhinitis (25 each), and 25 control participants. Total immunoglobulin (Ig) E and serum IFN-gamma were measured by enzyme-linked immunosorbent assay, the IFN-gamma polymorphism at position +874 was determined by amplification refractory mutation system-polymerase chain reaction, and eosinophil counts were recorded.
There was a significant association between genotype and the frequency of the A allele of the +874T/A polymorphism in atopic patients when compared with controls (P < .001). In all 3 groups, there was a significant increase in total IgE levels and eosinophil counts, and a decrease in serum IFN-gamma levels towards the presence of homozygous AA compared with homozygous TT.
The IFN-gamma gene polymorphism at position +874 contributes to susceptibility to atopic diseases by decreasing the amount of IFN-gamma. Identification of variants of IFN-gamma gene signalling and its role in the development of atopic diseases provides a focus for the development of novel diagnostic and therapeutic strategies for these diseases.
本研究旨在阐明干扰素(IFN)γ在特应性患者诊断及随访中的作用。我们对+874位点的IFN-γ多态性进行基因分型,以研究血清IFN-γ水平与疾病严重程度之间的关系,以及IFN-γ作为生化和免疫标志物的作用。
研究人群包括75例患有特应性哮喘、特应性皮炎和过敏性鼻炎的患者(各25例)以及25名对照参与者。采用酶联免疫吸附测定法检测总免疫球蛋白(Ig)E和血清IFN-γ,通过扩增阻滞突变系统-聚合酶链反应确定+874位点的IFN-γ多态性,并记录嗜酸性粒细胞计数。
与对照组相比,特应性患者中+874T/A多态性的A等位基因频率与基因型之间存在显著关联(P <.001)。在所有3组中,与纯合子TT相比,纯合子AA存在时总IgE水平和嗜酸性粒细胞计数显著增加,血清IFN-γ水平降低。
+874位点的IFN-γ基因多态性通过降低IFN-γ的量导致对特应性疾病的易感性。鉴定IFN-γ基因信号传导变体及其在特应性疾病发生中的作用为这些疾病新型诊断和治疗策略的开发提供了重点。