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Department of Immunology, University of Washington, Seattle, WA 98195
Recent evidence shows that many molecules of the TNF family serve as counter-receptors, inducing costimulation through reverse signals in addition to delivering signals through their respective TNF receptors. In this review, we will discuss this new class of costimulators with a focus on the mechanism of costimulation transduced by reverse signaling through Fas ligand.
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 Address correspondence and reprint requests to Dr. Pamela J. Fink, Department of Immunology, University of Washington, I-607H Health Sciences Center, Campus Box 357650, Seattle, WA, 98195. E-mail address: pfink{at}u.washington.edu
2 Abbreviations used in this paper: LT, lymphotoxin; CKI, casein kinase I; DC, dendritic cell; FasL, Fas ligand; HVEM, herpes simples virus entry mediator; LIGHT, homologous to lymphotoxin, exhibits inducible expression and competes with HSV glycoprotein D for HVEM, a receptor expressed on T cells; mTNF, membrane-bound TNF
; RANK, receptor activator of NF
B; SH3, Src homology 3; TNFR, TNF receptor; TRANCE, TNF-related activation-induced cytokine.
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