SEARCH:   Advanced

Blood, 1 January 2007, Vol. 109, No. 1, pp. 185-193. Prepublished online as a Blood First Edition Paper on September 7, 2006; DOI 10.1182/blood-2006-05-022954. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-05-022954v1 109/1/185    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 CrossRef Citing Articles via Google Scholar Google Scholar Articles by Jörgl, A. Articles by Strobl, H. Search for Related Content PubMed PubMed Citation Articles by Jörgl, A. Articles by Strobl, H. Related Collections Immunobiology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Human Langerhans-cell activation triggered in vitro by conditionally expressed MKK6 is counterregulated by the downstream effector RelB Almut Jörgl1, Barbara Platzer1, Sabine Taschner1, Leonhard X. Heinz1, Bernhard Höcher1, Peter M. Reisner1, Florian Göbel1, and Herbert Strobl1, 1 Institute of Immunology, Medical University Vienna, Austria Environmentally exposed epithelial Langerhans cells (LCs) encounter diverse innate stress signals, which lead to the activation of complex intracellular signaling cascades. Among these, p38 MAPK is consistently phosphorylated. For which aspects of LC activation triggering of p38 signaling is sufficient remains to be elucidated. We show that conditional induction of a dominant active form of MAPK kinase 6 (d.a.MKK6), a direct upstream kinase of p38, in LCs efficiently induces the up-regulation of costimulatory molecules and enhances their T-cell stimulatory capacity. These immediate effects showed no or only a minor requirement for classical NF-B signaling. Concomitant with LC activation, d.a.MKK6 induced the alternative NF-B member RelB, whose nuclear localization marks mature DCs. Specific inhibition of nuclear RelB during d.a.MKK6-induced LC activation further enhanced their maturation state. This observation was validated using the p38 activator anisomycin, thus suggesting a novel LC intrinsic control mechanism regulated by RelB. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

	Copyright © 2007 by American Society of Hematology         Online ISSN: 1528-0020