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Related Concept Videos

B Cell Activation and Differentiation01:24

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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
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Hybridoma technology is used for the large-scale production of monoclonal antibodies. Monoclonal antibodies bind to only a single antigenic determinant or epitope. Such antibodies are used in research, diagnostics, and disease therapy. The hybridoma technology established in 1975 by Georges Köhler and Cesar Milstein was awarded the Nobel Prize in Medicine in 1984 for revolutionizing research and therapy.
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Related Experiment Video

Updated: Dec 13, 2025

Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches
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Lsh/HELLS is required for B lymphocyte development and immunoglobulin class switch recombination.

Yafeng He1, Jianke Ren1, Xiaoping Xu1

  • 1Epigenetics Section, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702.

Proceedings of the National Academy of Sciences of the United States of America
|July 31, 2020
PubMed
Summary

Loss of HELLS/Lsh impairs B cell development and immunoglobulin production by affecting DNA repair during class switch recombination. This highlights Lsh

Keywords:
ICF syndromeLshchromatin remodelerclass switch recombination

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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Mutation of HELLS (Helicase, Lymphoid-Specific)/Lsh is linked to severe immunodeficiency syndromes.
  • The precise defect caused by Lsh mutation in hematopoiesis remains unclear.

Purpose of the Study:

  • To investigate the role of Lsh in hematopoiesis and B cell development.
  • To elucidate the molecular mechanisms underlying Lsh-associated immunodeficiency.

Main Methods:

  • Conditional Lsh knockout mice (using Mx1 or Vav Cre-recombinase) were generated.
  • Bone marrow transplantation studies were performed.
  • B lymphocyte function, including proliferation, immunoglobulin production, and class switch recombination (CSR), was assessed in vitro and in vivo.

Main Results:

  • Lsh depletion in hematopoietic stem cells led to reduced B cell numbers and impaired B cell development autonomously.
  • Lsh-deficient mice showed lower immunoglobulin levels despite normal peripheral B cell counts.
  • While CSR initiation was unaffected, Lsh-deficient B cells exhibited impaired canonical end-joining DNA repair pathways.

Conclusions:

  • Lsh plays a critical cell-intrinsic role in B cell development and class switch recombination.
  • Impaired DNA repair via the end-joining pathway is a key defect in Lsh-deficient B cells.
  • Lsh represents a potential therapeutic target for immunodeficiency disorders.