Human Langerhans-cell activation triggered in vitro by conditionally expressed MKK6 is counterregulated by the downstream effector RelB

Jorgl, Almut, Platzer, Barbara, Taschner, Sabine, Heinz, Leonhard X., Hocher, Bernhard, Reisner, Peter M., Gobel, Florian and Strobl, Herbert (2007) Human Langerhans-cell activation triggered in vitro by conditionally expressed MKK6 is counterregulated by the downstream effector RelB. Blood, 109 1: 185-193. doi:10.1182/blood-2006-05-022954


Author Jorgl, Almut
Platzer, Barbara
Taschner, Sabine
Heinz, Leonhard X.
Hocher, Bernhard
Reisner, Peter M.
Gobel, Florian
Strobl, Herbert
Title Human Langerhans-cell activation triggered in vitro by conditionally expressed MKK6 is counterregulated by the downstream effector RelB
Journal name Blood   Check publisher's open access policy
ISSN 0006-4971
1528-0020
Publication date 2007-01-01
Year available 2006
Sub-type Article (original research)
DOI 10.1182/blood-2006-05-022954
Volume 109
Issue 1
Start page 185
End page 193
Total pages 9
Place of publication Washington, DC, United States
Publisher American Society of Hematology
Language eng
Abstract 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-κB signaling. Concomitant with LC activation, d.a.MKK6 induced the alternative NF-κB 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. © 2007 by The American Society of Hematology.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown
Additional Notes Published online before print September 7, 2006

Document type: Journal Article
Sub-type: Article (original research)
Collection: Institute for Molecular Bioscience - Publications
 
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Created: Fri, 10 Jun 2011, 21:56:47 EST by Susan Allen on behalf of Institute for Molecular Bioscience