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Cell Immunol. 1998 May 25;186(1):55-62.

Strength of signal through BCR determines the fate of cycling B cells by regulating the expression of the Bcl-2 family of survival proteins.

Author information

1
Department of Microbiology and Immunology, University of Kentucky Medical Center, Lexington 40536-0084, USA.

Abstract

Cycling, splenic B cells were recultured with: (1) no stimulant to reflect poorly competitive clones; (2) soluble, whole anti-mu to reflect clones that bind soluble immune complexes; (3) soluble F(ab')2 anti-mu to reflect clones that bind soluble antigen; and (4) immobilized anti-mu to reflect clones that bind antigen presented by FDC. All four groups displayed similar levels of the death proteins Bax and Bcl-xS. In contrast, cycling B cells restimulated with either soluble F(ab')2 or immobilized anti-mu expressed heightened levels of the survival protein Bcl-xL, and only cells restimulated with immobilized anti-mu expressed the survival protein Bcl-2. Cycling B cells restimulated with either soluble F(ab')2 or immobilized anti-mu displayed a selective survival advantage over cycling B cells receiving no stimulus or soluble, whole anti-mu by both enhancing their responsiveness to CD40 ligand, a Th-cell-derived signal, and increasing the period that the cycling B cells remained responsive to this Th-cell-derived signal. The Th-cell-derived signal did not appreciably alter cycling B cell expression of Bcl-2 family members.

PMID:
9637765
DOI:
10.1006/cimm.1998.1292
[Indexed for MEDLINE]

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