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

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 (TNF-) 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- 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- 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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