体细胞突变
胞苷脱氨酶
生物
生发中心
获得性免疫系统
免疫系统
免疫球蛋白类转换
活化诱导(胞苷)脱氨酶
免疫学
阿波贝克
基因
抗体
遗传学
基因组
B细胞
作者
Meenal Choudhary,Anubhav Tamrakar,Amit Kumar Singh,Monika Jain,Ankit Jaiswal,Prashant Kodgire
标识
DOI:10.1080/08830185.2017.1369980
摘要
Activation-induced cytidine deaminase (AID), primarily expressed in activated mature B lymphocytes in germinal centers, is the key factor in adaptive immune response against foreign antigens. AID is responsible for producing high-affinity and high-specificity antibodies against an infectious agent, through the physiological DNA alteration processes of antibody genes by somatic hypermutation (SHM) and class-switch recombination (CSR) and functions by deaminating deoxycytidines (dC) to deoxyuridines (dU), thereby introducing point mutations and double-stranded chromosomal breaks (DSBs). The beneficial physiological role of AID in antibody diversification is outweighed by its detrimental role in the genesis of several chronic immune diseases, under non-physiological conditions. This review offers a comprehensive and better understanding of AID biology and its pathological aspects, as well as addresses the challenges involved in AID-related cancer therapeutics, based on various recent advances and evidence available in the literature till date. In this article, we discuss ways through which our interpretation of AID biology may reflect upon novel clinical insights, which could be successfully translated into designing clinical trials and improving patient prognosis and disease management.
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