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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Cassatella, M. A. Articles by Yoshimura, A. Search for Related Content PubMed PubMed Citation Articles by Cassatella, M. A. Articles by Yoshimura, A. Related Collections Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 94 No. 8 (October 15), 1999: pp. 2880-2889 Interleukin-10 (IL-10) Selectively Enhances CIS3/SOCS3 mRNA Expression in Human Neutrophils: Evidence for an IL-10-Induced Pathway That Is Independent of STAT Protein Activation Marco A. Cassatella, Sara Gasperini, Chiara Bovolenta, Federica Calzetti, Marieke Vollebregt, Patrizia Scapini, Martina Marchi, Ritsu Suzuki, Asuka Suzuki, and Akihiko Yoshimura From the Department of Pathology, University of Verona, Verona, Italy; the AIDS Immunopathogenesis Unit, San Raffaele Scientific Institute, Milano, Italy; and the Institute of Life Science, Kurume University, Aikawamachi, Kurume, Japan. We have recently shown that, in human neutrophils, interleukin-10 (IL-10) fails to induce specific DNA-binding activities to the gamma-interferon response region (GRR), a regulatory element located in the FcRI gene promoter, which is required for transcriptional activation by IL-10 and interferon  (IFN) in monocytic cells. In this study, we report that IL-10 is also unable to induce the binding of STAT1 or STAT3 to the serum-inducible element (hSIE/m67), despite the fact that both proteins are expressed in neutrophils. Whereas IFN and granulocyte colony-stimulating factor (G-CSF) are efficient inducers of STAT1 and STAT3 tyrosine phosphorylation in polymorphonuclear neutrophils (PMN), IL-10 fails to trigger STAT1 and STAT3 tyrosine and serine phosphorylation, therefore explaining its inability to induce the FcRI expression in these cells. By contrast, we demonstrate that IL-10 alone represents an efficient stimulus of CIS3/SOCS3 mRNA expression in neutrophils. CIS3/SOCS3 belongs to the recently cloned cytokine-inducible SH2-containing protein (CIS) gene family (which also includes CIS1, CIS2, CIS4, CIS5, and JAB) that is believed to be, at least in part, under the control of STAT transcription factors and whose products are potential modulators of cytokine signaling. Moreover, IL-10 synergizes with lipopolysaccharide (LPS) in upregulating CIS3/SOCS3 mRNA expression in PMN through a mechanism that involves mRNA stabilization. In contrast to CIS3/SOCS3, mRNA transcripts encoding other family members are unaffected by IL-10 in neutrophils. Finally, transfection of CIS3/SOCS3 in murine M1 myeloid cells suppresses LPS-induced growth arrest, macrophage-like differentiation, and nitric oxide synthesis, but not IL-6 mRNA expression. Collectively, our data suggest that, in neutrophils, the activation of STAT1 and STAT3 phosphorylation is neither required for CIS3/SOCS3 induction by IL-10 nor involved in the regulatory effects of IL-10 on cytokine production. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Miyazaki, C. H. Kuo, T. Tominaga, Y. Inoue, and S. J. Ono Regulatory Function of CpG-Activated B Cells in Late-Phase Experimental Allergic Conjunctivitis Invest. Ophthalmol. Vis. Sci., April 1, 2009; 50(4): 1626 - 1635. [Abstract] [Full Text] [PDF] Y. S. Lee, K. E. Latham, and C. A. 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