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Induction and Assessment of Class Switch Recombination in Purified Murine B Cells
09:49

Induction and Assessment of Class Switch Recombination in Purified Murine B Cells

Published on: August 14, 2010

Expression of activation-induced cytidine deaminase is regulated by cell division, providing a mechanistic basis for

James S Rush1, Man Liu, Valerie H Odegard

  • 1Howard Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, 300 Cedar Street, Box 208011, New Haven, CT 06520-8011, USA. jrush@gnf.org

Proceedings of the National Academy of Sciences of the United States of America
|September 6, 2005
PubMed

Insights

Class switch recombination (CSR) probability increases with cell division, not time. This is linked to rising activation-induced cytidine deaminase (AID) expression, which drives CSR in B cells.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • Class switch recombination (CSR) is a crucial process in adaptive immunity, enabling B cells to change antibody effector functions.
  • CSR isotype switching is influenced by B cell activation signals and cytokine exposure.
  • Recent studies suggest CSR probability correlates with cell division, independent of time.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying division-linked Class Switch Recombination (CSR).
  • To determine how cell division influences CSR by analyzing molecular features like Ig heavy chain accessibility and AID expression.

Main Methods:

  • Analysis of molecular features of CSR in relation to cell division.
  • Quantification of Ig heavy chain constant region accessibility.
  • Measurement of activation-induced cytidine deaminase (AID) mRNA expression across cell divisions.

Main Results:

  • Ig heavy chain accessibility for CSR was established after one cell division and remained constant.
  • Activation-induced cytidine deaminase (AID) mRNA expression increased with successive cell divisions, correlating with CSR frequency.
  • AID levels per division were time-independent, indicating division-linked regulation.

Conclusions:

  • The study proposes that increased AID expression with cell division is the molecular driver of division-linked CSR.
  • Constitutive AID expression accelerated division-linked CSR, supporting the proposed mechanism.
  • This finding provides a mechanistic explanation for how cell division influences B cell antibody class switching.

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