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Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation
09:02

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation

Published on: November 26, 2018

Expression of Ig-beta (CD79b) by chronic lymphocytic leukemia B cells that lack immunoglobulin heavy-chain allelic

L Z Rassenti1, T J Kipps

  • 1Division of Hematology/Oncology, Department of Medicine, University of California-San Diego, La Jolla, CA 92093-0663, USA.

Blood
|February 7, 2001
PubMed

Insights

Chronic lymphocytic leukemia (CLL) B cells with unusual immunoglobulin heavy-chain expression lack CD79b mutations. This suggests structural gene defects are not the cause of impaired immunoglobulin allelic exclusion in CLL.

Area of Science:

  • Immunology
  • Molecular Biology
  • Hematology

Background:

  • Immunoglobulin (Ig)-beta (CD79b) is crucial for immunoglobulin allelic exclusion.
  • Some chronic lymphocytic leukemia (CLL) B cells express multiple Ig heavy-chain alleles, failing normal allelic exclusion.
  • The molecular basis for this failure in CLL is not fully understood.

Purpose of the Study:

  • To investigate the role of CD79b structure and function in CLL B cells with aberrant Ig heavy-chain allelic expression.
  • To determine if mutations in CD79b are associated with the failure of immunoglobulin allelic exclusion in CLL.

Main Methods:

  • Analysis of CD79b expression on CLL samples using monoclonal antibodies.
  • Assessment of CD79b gene function in CLL cells.
  • Sequencing of CD79b genes to identify mutations, particularly in signal-transduction domains.

Main Results:

  • CLL samples, regardless of allelic exclusion status, showed poor staining for extracellular CD79b epitopes.
  • All examined CLL samples expressed functional CD79b genes.
  • Variant CD79b genes with conservative substitutions were found but were not specific to samples lacking allelic exclusion, suggesting genetic polymorphism.

Conclusions:

  • The failure of immunoglobulin heavy-chain allelic exclusion in CLL B cells is not linked to structural, nonconservative mutations in the signal-transduction domains of CD79b.
  • The findings suggest that aberrant CD79b expression or other regulatory mechanisms may be involved in the impaired allelic exclusion observed in CLL.

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