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© The Rockefeller University Press, 0022-1007/1998/3/847/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 6, March 16, 1998 847-853

Articles

Tolerant B Lymphocytes Acquire Resistance to Fas-mediated Apoptosis after Treatment with Interleukin 4 but Not after Treatment with Specific Antigen Unless a Surface Immunoglobulin Threshold Is Exceeded

Linda C. Foote*, Ann Marshak-Rothstein*,{ddagger}, and Thomas L. Rothstein*,§

From the * Department of Microbiology, the {ddagger} Department of Pathology, and the § Department of Medicine; and the §Evans Memorial Department of Clinical Research, Boston University Medical Center, Boston, Massachusetts 02118

Susceptibility to Fas-mediated apoptosis in nontolerant B cells is regulated in a receptor-specific fashion. To explore the regulation of Fas killing in tolerant, autoreactive B cells, mice doubly transgenic for hen egg lysozyme (HEL)–specific B cell receptors and soluble HEL were examined. Engagement of CD40 led to enhanced Fas expression and acquisition of sensitivity to Fas-mediated apoptosis in tolerant B cells, similar to that observed in nontolerant, receptor transgenic B cells. Engagement of surface immunoglobulin by specific (HEL) antigen failed to induce Fas resistance in tolerant B cells, in contrast to its effect on nontolerant B cells; however, cross-linking of biotinylated HEL with streptavidin induced similar levels of Fas resistance in tolerant and nontolerant B cells, which approximated the degree of Fas resistance produced by anti-Ig. Unlike surface Ig (sIg) engagement, physiological engagement of IL-4 receptors produced similar levels of Fas resistance in tolerant and nontolerant B cells. Thus, tolerant B cells differ from nontolerant B cells in the diminished capacity of surface immunoglobulin engagement to produce Fas resistance; however, tolerant B cells can be induced to become resistant to Fas-mediated apoptosis by IL-4 or by higher order cross-linking of sIg receptors.

Address correspondence to T.L. Rothstein, Boston Medical Center, Rm. E-556, 88 East Newton St., Boston, MA 02118; Phone: 617-638-7028; Fax: 617-638-7530; E-mail: trothstein{at}med-med1.bu.edu

1Abbreviations used in this paper: BCR, B cell antigen receptor; CD40L, soluble, chimeric CD40 ligand; DTg, double transgenic (anti-HEL/ HEL); HEL, hen egg lysozyme; rIL-4, recombinant mouse interleukin 4; sHEL, soluble hen egg lysozyme; sIg, surface Ig; STg, single transgenic (anti-HEL); Th1-CMC, Th1 cell-mediated cytotoxicity.

Linda Foote's current address is Department of Biology, Merrimack College, North Andover, MA 01834.


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