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CD28 Signaling Augments Elk-1-Dependent Transcription at the c-fos Gene During Antigen Stimulation¹

Wei Li^*, Carmella D. Whaley^*, Jody L. Bonnevier^*, Anna Mondino, Molly E. Martin^*, Kjersti M. Aagaard-Tillery^* and Daniel L. Mueller^2,*

^* Department of Medicine, Rheumatic and Autoimmune Diseases Section, and Center for Immunology, University of Minnesota Medical School, Minneapolis, MN 55455; and Department of Molecular Pathology and Medicine, Cancer Immunotherapy and Gene Therapy Program, DIBIT/H.S. Raffaele, Milan, Italy

Untransformed CD4⁺ Th1 cells stimulated with Ag and APC demonstrated a dependence on B7- and CD28-mediated costimulatory signals for the expression and function of AP-1 proteins. The induction of transactivation by the c-fos gene regulator Elk-1 mirrored this requirement for TCR and CD28 signal integration. c-Jun N-terminal kinase (JNK) (but not extracellular signal-regulated kinase or p38) protein kinase activity was similarly inhibited by neutralizing anti-B7 mAbs. Blockade of JNK protein kinase activity with SB 202190 prevented both Elk-1 transactivation and c-Fos induction. These results identify a unique role for B7 costimulatory molecules and CD28 in the activation of JNK during Ag stimulation in Th1 cells, and suggest that JNK regulates Elk-1 transactivation at the c-fos gene to promote the formation of AP-1 complexes important to IL-2 gene expression.

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