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Blood, 15 December 2003, Vol. 102, No. 13, pp. 4441-4447. Prepublished online as a Blood First Edition Paper on August 14, 2003; DOI 10.1182/blood-2002-11-3420. This Article Full Text 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 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 Guo, Z. Articles by Cao, X. Search for Related Content PubMed PubMed Citation Articles by Guo, Z. Articles by Cao, X. Related Collections Immunobiology Phagocytes Transplantation Apoptosis Signal Transduction Immunotherapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY 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 From the Institute of Immunology, Second Military Medical University, Shanghai; and the Institute of Immunology, Zhejiang University, Hangzhou, People's Republic of China. The mechanisms that underpin the intriguing capacity of Fas ligation on dendritic cells (DCs) 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 DCs, and we demonstrate that phenotypic maturation is associated with phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, activation of caspase-1, and secretion of interleukin- (IL-1). Specific inhibition of ERK1/2 diminished Fas ligation-induced caspase-1 activation, IL-1 secretion, and ensuing up-regulation of developmental markers, whereas treatment with neutralizing anti-IL-1 antibody abrogated phenotypic and functional maturation, indicating that IL-1 mediates Fas ligation-induced DC maturation in an autocrine manner. NF-B activation was responsible for maintaining DC viability after Fas ligation. Inhibiting NF-B did not affect either IL-1 secretion or phenotypic maturation but rather sensitized DCs to Fas-mediated apoptosis. In conclusion, positive signals originating from Fas are transduced through at least 2 different intracellular pathways in DCs, promoting not only survival but also an increase in maturation that correlates with increased antigen-presentation capability. (Blood. 2003;102:4441-4447) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Kawasaki, M. A. Choudhry, M. G. Schwacha, S. Fujimi, J. A. Lederer, K. I. Bland, and I. H. Chaudry Trauma-hemorrhage inhibits splenic dendritic cell proinflammatory cytokine production via a mitogen-activated protein kinase process Am J Physiol Cell Physiol, March 1, 2008; 294(3): C754 - C764. [Abstract] [Full Text] [PDF] Y. Jiang, G. Chen, Y. Zhang, L. Lu, S. Liu, and X. Cao Nerve Growth Factor Promotes TLR4 Signaling-Induced Maturation of Human Dendritic Cells In Vitro through Inducible p75NTR 1 J. Immunol., November 1, 2007; 179(9): 6297 - 6304. 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