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Prepublished online as a Blood First Edition Paper on August 14, 2003; DOI 10.1182/blood-2002-11-3420. This Article Full Text (PDF) All Versions of this Article: 2002-11-3420v1 102/13/4441    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 Guo, Z. Articles by Cao, X. Search for Related Content PubMed PubMed Citation Articles by Guo, Z. Articles by Cao, X. Social Bookmarking                   What's this? Submitted December 3, 2002 Accepted August 8, 2003 Fas ligation induces IL-1-dependent maturation and IL-1-independent survival of dendritic cells: different roles of ERK and NF-B signaling pathways Zhenhong Guo, Minghui Zhang, Huazhang An, Weilin Chen, Shuxun Liu, Jun Guo, Yizhi Yu, and Xuetao Cao* Institute of Immunology, Second Military Medical University, Shanghai, China; Institute of Immunology, Zhejiang University, Hangzhou, Zhejiang, China * Corresponding author; email: caoxt{at}public3.sta.net.cn. The mechanisms that underpin the intriguing capacity of Fas ligation on DC to induce maturation and activation, rather than apoptosis, remain unclear. In the present study we confirm that Fas signaling induces both phenotypic and functional maturation of murine DC, and demonstrate that phenotypic maturation is associated with phosphorylation of ERK1/2, activation of caspase 1 and secretion of IL-1beta. Specific inhibition of ERK1/2 diminished Fas ligation-induced caspase 1 activation, IL-1beta secretion and ensuing up-regulation of developmental markers, while treatment with neutralizing anti-IL-1beta antibody abrogated both phenotypic and functional maturation, indicating that IL-1beta mediates Fas ligation-induced DC maturation in an autocrine manner. NF-kappaB activation was responsible for maintenance of DC viability following Fas ligation. Inhibiting NF-kappaB did not affect either IL-1beta secretion or phenotypic maturation, but rather sensitized DC to Fas-mediated apoptosis. In conclusion, positive signals originating from Fas are transduced through at least two different intracellular pathways in DC, promoting not only survival, but also an increase in maturation that correlates with increased antigen presentation capability. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Kawasaki, M. A. 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