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Prepublished online as a Blood First Edition Paper on August 7, 2003; DOI 10.1182/blood-2003-04-1228. This Article Full Text (PDF) All Versions of this Article: 2003-04-1228v1 102/12/4123    most recent Alert me when this article is cited Alert me if a correction is posted 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 Kuwata, H. Articles by Akira, S. Search for Related Content PubMed PubMed Citation Articles by Kuwata, H. Articles by Akira, S. Social Bookmarking                   What's this? Submitted April 18, 2003 Accepted July 28, 2003 IL-10-inducible Bcl-3 negatively regulates LPS-induced TNF- production in macrophages Hirotaka Kuwata, Yasuyuki Watanabe, Hiroyuki Miyoshi, Masahiro Yamamoto, Tsuneyasu Kaisho, Kiyoshi Takeda, and Shizuo Akira* Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; ERATO, Japan Science and Technology Corporation, Osaka, Japan Subteam for Manipulation of Cell Fate, BioResource Center, RIKEN Tsukuba Institute, Tsukuba, Japan Laboratory of Host Defense, RIKEN Research Center for Allergy and Immunology, Yokohama, Japan * Corresponding author; email: sakira{at}biken.osaka-u.ac.jp. Interleukin-10 (IL-10) plays an important role in prevention of chronic inflammation in vivo. However, the molecular mechanism by which IL-10 exerts its anti-inflammatory response is poorly understood. Here, we performed a microarray analysis and identified Bcl-3 as an IL-10-inducible gene in macrophages. Lentiviral vector-mediated expression of Bcl-3 inhibited LPS-induced production of TNF-, but not IL-6, in macrophages. In Bcl-3-transduced and IL-10-pretreated macrophages, LPS-induced nuclear translocation of NF-B p65 was not impaired. However, DNA binding by NF-B p50/p65 was profoundly inhibited. Nuclear localization of Bcl-3 was associated with inhibition of LPS-induced TNF- production. Overexpression of Bcl-3 suppressed activation of the TNF- promoter, but not the IL-6 promoter. Bcl-3 interacted with NF-B p50 and was recruited to the TNF- promoter, but not the IL-6 promoter, indicating that Bcl-3 facilitates p50-mediated inhibition of TNF- expression. Furthermore, Bcl-3-deficient macrophages showed defective IL-10-mediated suppression of LPS induction of TNF-, but not IL-6. These findings suggest that IL-10-induced Bcl-3 is required for suppression of TNF- production in macrophages. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? 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