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The Journal of Immunology, 1999, 162: 6317-6321.
Copyright © 1999 by The American Association of Immunologists

Inhibition of B Cell Receptor-Mediated Apoptosis by IFN1

Leon Su and Michael David2

Department of Biology and University of California, San Diego, Cancer Center, La Jolla, CA 92093

IFNs are a family of cytokines that are involved in the regulation of immune and inflammatory responses. Clinical use of IFN-{alpha}/ß encompasses treatment for a variety of diseases; however, prolonged exposure to IFN-{alpha}/ß results in elevated levels of autoreactive Abs. In this study, we investigated the potential of IFNs to modulate apoptotic signals in B cells. We demonstrate that IFN-{alpha} or IFN-ß inhibit Ag receptor-mediated apoptosis in a dose-dependent manner. Inhibition of phosphatidylinositol 3' (PI3)-kinase did not abolish the effect of IFN, indicating that the antiapoptotic mechanism is PI3-kinase- and protein kinase B/Akt-independent. Instead, IFN-{alpha} and IFN-ß, but not IFN-{gamma}, significantly increase the levels of the survival protein Bcl-2, and to a lesser extent, Bcl-xL expression. Thus, IFN-{alpha}/ß-mediated inhibition of B cell Ag receptor-triggered apoptosis may offer a model for the process that leads to the escape of self-reactive B cells from negative selection and consequently results in autoantibody production.




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