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Apoptosis in B lymphocytes: the WEHI-231 perspective
1Department of Pathology and Cancer Research Center, University of Chicago, IL 60637, USA.
Immunology and Cell Biology
|February 1, 1995
Summary
The murine B cell lymphoma WEHI-231 undergoes apoptosis upon antigen receptor cross-linking, mediated by ceramide. Variants resistant to this process still possess intact apoptotic machinery, suggesting complex regulatory mechanisms.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- The WEHI-231 murine B cell lymphoma model is used to study apoptosis.
- Apoptosis in these cells can be triggered by cross-linking the surface IgM (sIgM) antigen receptor.
- Cell cycle arrest precedes apoptosis, and subline variations exist.
Purpose of the Study:
- To review recent work on the molecular basis of apoptosis in WEHI-231 cells.
- To understand the signaling pathway leading to apoptosis upon anti-Ig treatment.
- To investigate the role of ceramide in mediating apoptosis.
Main Methods:
- Review of existing literature on WEHI-231 cell apoptosis.
- Analysis of WEHI-231 sublines with varying sensitivities to anti-Ig treatment.
- Assessment of apoptotic machinery integrity in resistant variants.
Main Results:
- Anti-Ig treatment induces apoptosis specifically via sIgM, not sIgD, Ia, or FcR.
- Apoptosis-resistant WEHI-231 variants retain sensitivity to other apoptotic stimuli like dexamethasone and irradiation.
- Ceramide, a sphingosine derivative, is identified as the mediator of apoptosis in susceptible cells.
Conclusions:
- WEHI-231 apoptosis is regulated by short-lived protein inhibitors that are removed upon anti-Ig treatment.
- Ceramide production, likely via membrane sphingomyelinases, is crucial for initiating apoptosis.
- A hypothetical model for ceramide-induced apoptosis in WEHI-231 cells is proposed.
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