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Fas Apoptosis Inhibitory Molecule Enhances CD40 Signaling in B Cells and Augments the Plasma Cell Compartment¹

Center for Oncology and Cell Biology, The Feinstein Institute for Medical Research, Manhasset, NY 11030

Fas apoptosis inhibitory molecule (FAIM) was cloned as a mediator of Fas resistance that is highly evolutionarily conserved but contains no known effector motifs. In this study, we report entirely new functions of FAIM that regulate B cell signaling and differentiation. FAIM acts to specifically enhance CD40 signaling for NF-B activation, IRF-4 expression, and BCL-6 down-regulation in vitro, but has no effect on its own or in conjunction with LPS or anti-Ig stimulation. In keeping with its effects on IRF-4 and BCL-6, FAIM overexpression augments the plasma cell compartment in vivo. These results indicate that FAIM is a new player on the field of B cell differentiation and acts as a force multiplier for a series of events that begins with CD40 engagement and ends with plasma cell differentiation.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by United States Public Health Service grant AI40181 awarded by the National Institute of Health in part by USPHS Grant AI40181.

² Address correspondence and reprint requests to Dr. Thomas L. Rothstein, Center for Oncology and Cell Biology (Immunobiology Laboratory), The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030. E-mail address: tr{at}nshs.edu

³ Abbreviations used in this paper: FAIM, fas apoptosis inhibitory molecule; BCL-6, B cell lymphoma-6; Blimp-1, B lymphocyte-induced maturation protein 1; EMSA, electrophoretic mobility shift assay; FAIM-L, FAIM-Long; FAIM-S, FAIM-Short; GC, germinal center; IRF, IFN regulatory factor; NGF, nerve growth factor; PAX-5, paired box gene 5; XBP-1, X-box binding protein 1.

This article has been cited by other articles:

				H. Kaku and T. L. Rothstein Fas Apoptosis Inhibitory Molecule Expression in B Cells Is Regulated through IRF4 in a Feed-Forward Mechanism J. Immunol., November 1, 2009; 183(9): 5575 - 5581. [Abstract] [Full Text] [PDF]