首页|Molecular mechanisms of DNA lesion and repair during antibody somatic hypermutation
Molecular mechanisms of DNA lesion and repair during antibody somatic hypermutation
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Antibody diversification is essential for an effective immune response,with somatic hypermutation(SHM)serving as a key molecular process in this adaptation.Activation-induced cytidine deaminase(AID)initiates SHM by inducing DNA lesions,which are ultimately resolved into point mutations,as well as small insertions and deletions(indels).These mutational outcomes contribute to antibody affinity maturation.The mechanisms responsible for generating point mutations and indels involve the base excision repair(BER)and mismatch repair(MMR)pathways,which are well coordinated to maintain genomic integrity while allowing for beneficial mutations to occur.In this regard,translesion synthesis(TLS)polymerases contribute to the diversity of mutational outcomes in antibody genes by enabling the bypass of DNA lesions.This review summarizes our current understanding of the distinct molecular mechanisms that generate point mutations and indels during SHM.Understanding these mechanisms is critical for elucidating the development of broadly neutralizing antibodies(bnAbs)and autoantibodies,and has implications for vaccine design and therapeutics.
somatic hypermutation(SHM)insertions and deletions(indels)AIDbase excision repair(BER)mismatch repair(MMR)translesion synthesis(TLS)polymerases
Qian Hao、Jinfeng Li、Leng-Siew Yeap
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Shanghai Institute of Immunology,Department of Immunology and Microbiology,State Key Laboratory of Oncogenes and Related Genes,Shanghai Jiao Tong University School of Medicine,Shanghai 200025,China
Center for Immune-Related Diseases at Shanghai Institute of Immunology,Department of Endocrinology and Metabolic Diseases,Ruijin Hospital,Shanghai Jiao Tong University School of Medicine,Shanghai 200025,China
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