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Related Collections Immunobiology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 October 2001, Vol. 98, No. 7, pp. 2175-2182 IMMUNOBIOLOGY Extracellular signal-regulated protein kinase signaling pathway negatively regulates the phenotypic and functional maturation of monocyte-derived human dendritic cells Amaya Puig-Kröger, Miguel Relloso, Oskar Fernández-Capetillo, Ana Zubiaga, Augusto Silva, Carmelo Bernabéu, and Angel L. Corbí From Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas; and Departamento de Biología Animal y Genética, Facultad de Ciencias, Universidad del Pais Vasco, Madrid, Spain. Dendritic cells (DC) are highly specialized antigen-presenting cells that on activation by inflammatory stimuli (eg, tumor necrosis factor  [TNF-] and interleukin-1 [IL-1]) or infectious agents (eg, lipopolysaccharide [LPS]), mature and migrate into lymphoid organs. During maturation, DC acquire the capacity to prime and polarize resting naive T lymphocytes. Maturation of monocyte-derived DC (MDDC) is inhibited by the p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580. This study found that in the presence of the mitogen-activated protein kinase kinase 1-extracellular signal-regulated kinase (ERK) inhibitors PD98059 or U0126, TNF-- and LPS-induced phenotypic and functional maturation is enhanced. ERK pathway inhibitors increased expression of major histocompatibility complex and costimulatory molecules; loss of mannose-receptor-mediated endocytic activity; nuclear factor-B DNA-binding activity; release of IL-12 p40; and allogeneic T-cell proliferation induced by LPS or TNF-. Moreover, PD98059 and U0126 enhanced LPS-triggered production of IL-12 p70. In agreement with the effect of ERK inhibitors, maturation of MDDC was delayed in the presence of serum, an effect that was reversed by U0126. These results indicate that the ERK and p38 MAPK signaling pathways differentially regulate maturation of MDDC and suggest that their relative levels of activation might modulate the initial commitment of naive T-helper (Th) cells toward Th1 or Th2 subsets. The findings also suggest that maturation of MDDC might be pharmacologically modified by altering the relative levels of activation of both intracellular signaling routes. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. A. Fulcher, M. H. Chang, S. Wang, T. Almazan, S. T. Hashimi, A. U. Eriksson, X. Wen, M. Pang, L. G. Baum, R. R. Singh, et al. Galectin-1 Co-clusters CD43/CD45 on Dendritic Cells and Induces Cell Activation and Migration through Syk and Protein Kinase C Signaling J. Biol. Chem., September 25, 2009; 284(39): 26860 - 26870. [Abstract] [Full Text] [PDF] S. M. Makela, M. Strengell, T. E. 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