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The Journal of Immunology, Vol 155, Issue 8 3830-3838, Copyright © 1995 by American Association of Immunologists
ARTICLES |
R Merino, DA Grillot, PL Simonian, S Muthukkumar, WC Fanslow, S Bondada and G Nunez
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109, USA.
The demise of B cell progenitors expressing functional IgM receptors for self appears to be the main mechanism by which B cell tolerance is accomplished. The genetic mechanisms that regulate the death process during this critical step of B cell development are still poorly understood. We have studied the regulation of apoptosis in WEHI-231 lymphoma cells after treatment with a panel of anti-IgM mAbs as an in vitro model of clonal B cell deletion. We showed that a product of bcl- x, Bcl-xL, can inhibit anti-IgM-induced apoptosis but not cell cycle arrest in a dose-dependent manner. Bcl-xL was efficient in protecting B cells from low but not high avidity anti-IgM mAbs. In contrast to that observed with Bcl-xL, CD40 stimulation was efficient in inhibiting both cell cycle arrest and apoptosis after IgM cross-linking regardless of the binding avidity of the anti-IgM Ab. Moreover, activation through IgM receptors but not CD40 induced up-regulation followed by rapid down- modulation of Bcl-xL. Thus, the capacity of Bcl-xL to modulate anti-IgM- induced apoptosis in WEHI-231 cells is highly dependent on the avidity of the Ab-IgM receptor interaction.
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