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伊朗人群中CCR5启动子多态性和CCR5 Δ 32突变的频率。

The frequency of CCR5 promoter polymorphisms and CCR5 Δ 32 mutation in Iranian populations.

作者信息

Zare-Bidaki Mohammad, Karimi-Googheri Masoud, Hassanshahi Gholamhossein, Zainodini Nahid, Arababadi Mohammad Kazemi

机构信息

Immunology of Infectious Diseases Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

Department of Immunology, Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.

出版信息

Iran J Basic Med Sci. 2015 Apr;18(4):312-6.

Abstract

Evidence showed that chemokines serve as pro-migratory factors for immune cells. CCL3, CCL4 and CCL5, as the main CC chemokines subfamily members, activate immune cells through binding to CC chemokine receptor 5 or CCR5. Macrophages, NK cells and T lymphocytes express CCR5 and thus, affected CCR5 expression or functions could be associated with altered immune responses. Deletion of 32 base pairs (Δ 32) in the exon 1 of the CCR5 gene, which is known as CCR5 Δ 32 mutation causes down regulation and malfunction of the molecule. Furthermore, it has been evidenced that three polymorphisms in the promoter region of CCR5 modulate its expression. Altered CCR5 expression in microbial infection and immune related diseases have been reported by several researchers but the role of CCR5 promoter polymorphisms and CCR5 Δ 32 mutation in Iranian patients suffering from these diseases are controversial. Due to the fact that Iranian people have different genetic backgrounds compared to other ethnics, hence, CCR5 promoter polymorphisms and CCR5 32 mutation association with the diseases may be different in Iranian patients. Therefore, this review addresses the most recent information regarding the prevalence as well as association of the mutation and polymorphisms in Iranian patients with microbial infection and immune related diseases as along with normal population.

摘要

证据表明趋化因子是免疫细胞的促迁移因子。CCL3、CCL4和CCL5作为主要的CC趋化因子亚家族成员,通过与CC趋化因子受体5(CCR5)结合来激活免疫细胞。巨噬细胞、自然杀伤细胞和T淋巴细胞表达CCR5,因此,CCR5表达或功能的改变可能与免疫反应的改变有关。CCR5基因外显子1中32个碱基对的缺失(Δ32),即所谓的CCR5 Δ32突变,会导致该分子的下调和功能异常。此外,已有证据表明CCR5启动子区域的三种多态性调节其表达。几位研究人员报告了微生物感染和免疫相关疾病中CCR5表达的改变,但CCR5启动子多态性和CCR5 Δ32突变在伊朗这些疾病患者中的作用存在争议。由于伊朗人与其他种族相比具有不同的遗传背景,因此,CCR5启动子多态性和CCR5 32突变与疾病的关联在伊朗患者中可能有所不同。因此,本综述阐述了有关伊朗患者以及正常人群中微生物感染和免疫相关疾病的CCR5突变和多态性的患病率及关联的最新信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/657c/4439444/afbf6c9d2a42/IJBMS-18-312-g001.jpg

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