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Murine Model of CD40-activation of B cells
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Expression of CD40 induces neural apoptosis
Y Ruan1, S Rabizadeh, D Camerini
1Department of Neurology, University of California, Los Angeles, USA.
Journal of Neuroscience Research
|November 19, 1997
Summary
Tumor necrosis factor receptor superfamily members CD40 and p75NTR can induce neural apoptosis. Apoptosis is inhibited by ligand or antibody binding, suggesting a dual role for these receptors in cell death regulation.
Area of Science:
- Cell Biology
- Immunology
- Neuroscience
Background:
- The tumor necrosis factor receptor superfamily (TNFRSF) comprises 12 members involved in diverse cellular processes.
- Some TNFRSF members, like tumor necrosis factor receptor I and FAS, mediate ligand-induced cell death.
- The neurotrophin receptor p75NTR induces neural apoptosis, which is inhibited by ligand binding, suggesting its role in neurotrophin dependence.
Purpose of the Study:
- To investigate the role of CD40, a TNFRSF member structurally related to p75NTR, in neural apoptosis.
- To determine if CD40 signaling, similar to p75NTR, can induce apoptosis and whether this process is modulated by ligand or antibody binding.
Main Methods:
- Utilized a model system to study neural apoptosis induced by CD40.
- Investigated the effect of G28-5 monoclonal antibody binding on CD40-mediated apoptosis.
Main Results:
- CD40 was shown to induce neural apoptosis, mirroring the function of p75NTR.
- Binding of the G28-5 monoclonal antibody to CD40 inhibited the induced neural apoptosis.
- These findings suggest that CD40, like p75NTR, can mediate apoptosis in a ligand-independent manner, with inhibition by binding.
Conclusions:
- Results support a model where certain TNFRSF members induce apoptosis upon ligand binding, while others, like CD40 and p75NTR, can induce apoptosis independently of ligand.
- Apoptosis mediated by these receptors can be inhibited by the binding of specific ligands or monoclonal antibodies.
- This highlights a complex regulatory mechanism within the TNFRSF concerning cell death pathways.
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