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B Cell Activation and Differentiation

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

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

Published on: November 26, 2018

Functional Differences between IgM and IgD Signaling in Chronic Lymphocytic Leukemia.

Elisa Ten Hacken¹, Mariela Sivina¹, Ekaterina Kim¹

¹Department of Leukemia, University of Texas MD Anderson Cancer Center, Houston, TX 77230;

Journal of Immunology (Baltimore, Md. : 1950)

|August 19, 2016

Summary

Chronic lymphocytic leukemia (CLL) B-cell receptor (BCR) signaling differs between IgM and IgD isotypes. IgM promotes CLL cell survival and chemokine secretion, while IgD signaling leads to receptor internalization and inhibits these responses.

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Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients

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Published on: June 16, 2017

Area of Science:

Immunology
Hematology
Molecular Biology

Background:

B-cell receptor (BCR) signaling is crucial in chronic lymphocytic leukemia (CLL) pathogenesis.
CLL cells primarily express IgM and IgD BCR isotypes, but their distinct functional roles are not fully understood.

Purpose of the Study:

To investigate and compare the functional outcomes of IgM and IgD BCR signaling in CLL cells.
To explore these signaling differences in both freshly isolated cells and a microenvironment-mimicking model.

Main Methods:

Analysis of signaling pathways (ERK, HS1, F-actin) in CLL cells stimulated via IgM or IgD.
Assessment of downstream functional responses: cell survival, chemokine secretion (CCL3, CCL4), and receptor expression.
Coculture of CLL cells with nurselike cells to simulate the lymph node microenvironment.
Evaluation of the effect of Bruton's tyrosine kinase (BTK) inhibitor ibrutinib on BCR signaling.

Main Results:

IgM signaling induced sustained ERK activation, promoted CLL cell survival, and increased CCL3/CCL4 chemokine secretion.
IgD signaling triggered HS1 activation and F-actin polymerization, leading to rapid BCR internalization and impaired downstream signaling.
Distinct IgM and IgD signaling outcomes were observed in both isolated CLL cells and cocultured cells.
Ibrutinib effectively inhibited both IgM and IgD BCR signaling pathways.

Conclusions:

IgM and IgD BCR isotypes elicit significantly different functional responses in CLL cells.
These findings provide new insights into BCR signaling regulation in CLL and its potential therapeutic targeting.