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Cell Growth & Differentiation Vol. 13, 13-18, January 2002
© 2002 American Association for Cancer Research

Tumor Necrosis Factor {alpha} (TNF-{alpha}) Activates Jak1/Stat3-Stat5B Signaling through TNFR-1 in Human B Cells1

Sebastiano Miscia2, Marco Marchisio, Alfredo Grilli, Valentina Di Valerio, Lucia Centurione, Giuseppe Sabatino, Francesco Garaci, Giorgio Zauli, Ezio Bonvini and Angela Di Baldassarre

Cell Signaling Unit at the Department of Biomorphology [S. M., M. M., A. G., V. D. V., L. C., A. D. B.] and Section of Neonatology [G. S.], School of Medicine, University of Chieti, 66100 Chieti, Italy; Dipartimento di diagnostica per immagini e Radiologia Interventistica, University of Roma Tor Vergata, D0100 Rome, Italy [F. G.]; Section of Human Anatomy at the Department of Morphology and Embryology, University of Ferrara, 44100 Ferrara, Italy [M. M.]; Department of Human Morphology, School of Medicine, University of Trieste, 34127 Trieste, Italy [G. Z.]; and Laboratory of Immunobiology, Center for Biologistics Evaluation and Research, Bethesda, Maryland 20814 [E. B.]

The biological actions of tumor necrosis factor {alpha} (TNF-{alpha}) are mediated by two cell surface receptors, TNFR-1 and TNFR-2. These receptors do not display protein tyrosine kinase activity. Nevertheless, an early TNF-induced activation of specific tyrosine kinases has been reported as an important cue to the cellular response to this cytokine. Here we present evidence that TNF-{alpha} induces the activation of the cytoplasmic Janus tyrosine kinases Jak1 and Tyk2 in both human healthy peripheral and lymphoma B cells. This event was accompanied by the recruitment of a specific set of latent cytosolic transcription factors, Stat3 and Stat5b. Furthermore, Jak1 coprecipitated with TNFR-1 after TNF-{alpha} treatment. These data suggest that at least in human B cells this cytokine can exert its biological effects through the Jak-Stat signaling pathway and that such signals are initiated through an interaction between TNFR-1 and Jak 1.




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