| Literature DB >> 28933967 |
Meenal Choudhary1, Anubhav Tamrakar1, Amit Kumar Singh1, Monika Jain1, Ankit Jaiswal1, Prashant Kodgire1.
Abstract
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.Entities:
Keywords: Activation-induced cytidine deaminase (AID); chromosomal translocations; class-switch recombination (CSR); lymphoma; somatic hypermutation (SHM)
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Year: 2017 PMID: 28933967 DOI: 10.1080/08830185.2017.1369980
Source DB: PubMed Journal: Int Rev Immunol ISSN: 0883-0185 Impact factor: 5.311