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The Journal of Immunology, 1998, 161: 1183-1193.
Copyright © 1998 by The American Association of Immunologists

TNF Receptor-Associated Factor-3 Signaling Mediates Activation of p38 and Jun N-Terminal Kinase, Cytokine Secretion, and Ig Production Following Ligation of CD40 on Human B Cells1

Amrie C. Grammer*, Jennifer L. Swantek{dagger}, Richard D. McFarland{ddagger}, Yasushi Miura*, Thomas Geppert* and Peter E. Lipsky2,*

* Harold C. Simmons Arthritis Research Center and Departments of Internal Medicine, {dagger} Pharmacology, and {ddagger} Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75235

CD40 engagement induces a variety of functional outcomes following association with adaptor molecules of the TNF receptor-associated factor (TRAF) family. Whereas TRAF2, -5, and -6 initiate NF-{kappa}B activation, the outcomes of TRAF3-initiated signaling are less characterized. To delineate CD40-induced TRAF3-dependent events, Ramos B cells stably transfected with a dominant negative TRAF3 were stimulated with membranes expressing recombinant CD154/CD40 ligand. In the absence of TRAF3 signaling, activation of p38 and control of Ig production were abrogated, whereas Jun N-terminal kinase activation and secretion of IL-10, lymphotoxin-{alpha}, and TNF-{alpha} were partially blocked. By contrast, induction of apoptosis, activation of NF-{kappa}B, generation of granulocyte-macrophage CSF, and up-regulation of CD54, MHC class II, and CD95 were unaffected by the TRAF3 dominant negative. Together, these results indicate that TRAF3 initiates independent signaling pathways via p38 and JNK that are associated with specific functional outcomes.




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