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

doi:10.1084/jem.187.6.847

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J. Exp. Med., Volume 187, Number 6, March 16, 1998 847-853

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

By Linda C. Foote,^* Ann Marshak-Rothstein,^* and Thomas L. Rothstein^*^§

From the ^* Department of Microbiology, the 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 theregulation of Fas killing in tolerant, autoreactive B cells, micedoubly transgenic for hen egg lysozyme (HEL)-specific B cell receptorsand soluble HEL were examined. Engagement of CD40 led to enhancedFas expression and acquisition of sensitivity to Fas-mediatedapoptosis in tolerant B cells, similar to that observed in nontolerant,receptor transgenic B cells. Engagement of surface immunoglobulinby specific (HEL) antigen failed to induce Fas resistance in tolerantB cells, in contrast to its effect on nontolerant B cells; however,cross-linking of biotinylated HEL with streptavidin induced similarlevels 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 ofIL-4 receptors produced similar levels of Fas resistance in tolerantand nontolerant B cells. Thus, tolerant B cells differ from nontolerantB cells in the diminished capacity of surface immunoglobulin engagementto produce Fas resistance; however, tolerant B cells can be inducedto become resistant to Fas-mediated apoptosis by IL-4 or by higherorder cross-linking of sIg receptors.

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