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Related Concept Videos

Diversity of Antigen Receptors01:28

Diversity of Antigen Receptors

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Antigen receptors are essential components of the immune system crucial in defending the body against foreign invaders. These receptors are present on the surface of B and T cells, enabling them to recognize antigens and mount an appropriate immune response.
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Related Experiment Video

Updated: Aug 1, 2025

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches
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Mesoscale DNA feature in antibody-coding sequence facilitates somatic hypermutation.

Yanyan Wang1, Senxin Zhang2, Xinrui Yang3

  • 1State Key Laboratory of Molecular Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai 200031, China; 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.

Cell
|April 25, 2023
PubMed
Summary
This summary is machine-generated.

Somatic hypermutation (SHM) focuses on antibody genes due to DNA flexibility near the activation-induced cytidine deaminase (AID) enzyme. This flexibility guides mutations, enhancing antibody diversity and aiding lymphoma research.

Keywords:
AIDaffinity maturationcomplementarity-determining regiondeaminasesomatic hypermutation

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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Somatic hypermutation (SHM) is crucial for antibody affinity maturation.
  • The precise targeting of SHM to antibody complementarity-determining regions (CDRs) is not fully understood.
  • Activation-induced cytidine deaminase (AID) initiates SHM by deaminating DNA.

Purpose of the Study:

  • To elucidate the mechanism determining the specificity of AID-initiated mutations in antibody genes.
  • To investigate the role of DNA sequence and structure in directing SHM.
  • To explore the implications for antibody discovery and lymphoma pathogenesis.

Main Methods:

  • In vitro deaminase assays using varying DNA substrates.
  • Analysis of mesoscale DNA sequence features surrounding AID motifs.
  • In vivo mutational analysis in mouse models.
  • Evolutionary conservation analysis of SHM patterns.

Main Results:

  • DNA substrate flexibility, dictated by mesoscale sequences, governs AID binding and deamination.
  • Pyrimidine-pyrimidine sequences enhance AID activity by interacting with its charged surface.
  • CDR hypermutability can be mimicked in vitro and is evolutionarily conserved.
  • Altering mesoscale sequences modifies in vivo mutability and promotes mutations in specific regions.

Conclusions:

  • Antibody gene sequences possess intrinsic features that direct AID mutagenesis through DNA flexibility.
  • Mesoscale sequence properties play a critical role in determining SHM patterns.
  • Findings offer insights into antibody engineering, humanized animal models, and lymphoma development.