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Difference in apoptosis induction between surface IgD and IgM.

D Peckham¹, E Andersen-Nissen, F D Finkelman

¹Department of Medicine, Iowa City Veterans Administration Medical Center, Iowa City, IA 52242, USA.

International Immunology

|February 27, 2001

Summary

Low-dose anti-delta antibodies trigger B cell apoptosis, unlike anti-mu antibodies. This suggests a distinct B cell receptor signaling pathway influencing cell fate and immune tolerance.

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Area of Science:

Immunology
Cell Biology
Molecular Biology

Background:

The canonical two-signal model posits B cell activation requires antigen receptor (signal 1) and co-stimulatory signals (signal 2).
Signal 1 alone typically induces tolerance or anergy, while signal 1 plus signal 2 promotes proliferation.
The differential roles of B cell receptor (BCR) isotypes, like delta and mu, in regulating these outcomes remain incompletely understood.

Purpose of the Study:

To investigate the distinct effects of anti-delta versus anti-mu antibody stimulation on resting B cells.
To determine if BCR signal 1 alone can induce apoptosis in B cells.
To elucidate the molecular events associated with anti-delta-induced B cell apoptosis.

Main Methods:

Purified resting B cells from mice were treated with various concentrations of anti-delta or anti-mu antibodies in vitro.
Cell cycle entry (S phase), apoptosis, and expression of co-stimulatory molecules (B7-2, MHC class II) and transcription factors (c-Myc, Egr-1) were assessed.
Effects of co-stimulatory signals (anti-CD40, IL-4) on anti-delta-treated B cells were evaluated.

Main Results:

Low-dose anti-delta (0.1-0.5 µg/ml) induced accelerated apoptosis in B cells without significant cell cycle entry.
In contrast, anti-mu antibodies did not induce early apoptosis; higher doses of anti-delta (50 µg/ml) caused modest proliferation.
Anti-delta treatment upregulated B7-2 and MHC class II on apoptotic B cells and induced transient c-Myc/Egr-1 expression, a pattern linked to apoptosis.

Conclusions:

Cross-linking the delta BCR, but not the mu BCR, with low-dose antigen receptor stimulation can lead to B cell apoptosis.
A B cell receptor stimulus sufficient for early activation events but insufficient for full cell cycle entry may trigger programmed cell death.
These findings reveal a functional divergence between delta and mu BCR signaling in resting B cells, impacting immune tolerance.