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Bcl-x protects primary B cells against Fas-mediated apoptosis
T J Schneider1, D Grillot, L C Foote
1Department of Microbiology, Boston University Medical Center, MA 02118, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|November 20, 1997
Summary
B cells can resist Fas-mediated apoptosis when stimulated via surface immunoglobulin (Ig). This resistance is linked to increased Bcl-x protein, a key factor in cell survival pathways.
Area of Science:
- Immunology
- Molecular Biology
- Cell Death Research
Background:
- Primary murine splenic B cells exhibit variable sensitivity to Fas-mediated apoptosis.
- Stimulation via CD40 renders B cells Fas-sensitive, but surface Ig signaling confers resistance.
- This protective mechanism requires time and macromolecular synthesis, suggesting induced gene products.
Purpose of the Study:
- To investigate the role of Bcl-x in mediating resistance to Fas-mediated apoptosis in B cells.
- To examine the expression and function of Bcl-x following surface Ig cross-linking.
Main Methods:
- Primary murine splenic B cells were stimulated via CD40 and/or surface Ig (anti-IgM).
- Bcl-x messenger RNA (mRNA) and protein expression levels were analyzed.
- Fas-mediated apoptosis sensitivity was assessed in wild-type and Bcl-x transgenic (Tg) B cells.
Main Results:
- Anti-IgM treatment induced bcl-x mRNA and Bcl-x protein in otherwise Fas-sensitive B cells.
- Bcl-x protein induction correlated with the onset of resistance to Fas-mediated apoptosis.
- B cells from Bcl-x Tg mice demonstrated resistance to Fas-mediated apoptosis.
Conclusions:
- Increased Bcl-x expression is a key mediator of protection against Fas-mediated apoptosis induced by surface Ig cross-linking in B cells.
- This finding highlights the role of Bcl-x in regulating B cell survival and immune responses.