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Mhc class ii engagement in brain endothelial cells induces protein kinase a-dependent il-6 secretion and phosphorylation of camp response element-binding protein

Academic Article
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Overview

authors

  • Etienne, S.
  • Bourdoulous, S.
  • Strosberg, Donny
  • Courand, P. O.

publication date

  • October 1999

journal

  • Journal of Immunology  Journal

abstract

  • Activated endothelial cells can directly participate in immune responses by interacting with immunocompetent cells via class II MHC proteins. We show here that, after induction of MHC class II molecule expression by IFN-gamma, rat brain endothelial cells responded to MHC class II ligands, anti-MHC class II Abs, or superantigens by expression of IL-6 transcript and IL-6 secretion. This response was not affected by protein kinase C depletion but was mimicked by the cAMP-elevating agent forskolin and completely blocked by H89, an inhibitor of cAMP-dependent protein kinase (PKA). Involvement of a cAMP/PKA signaling pathway in response to MHC class II ligands was further demonstrated by measure of a dose-dependent increase in cAMP level and phosphorylation of the transcription factor cAMP response element-binding protein (CREB). Our results indicate that MHC class II engagement in brain endothelial cells is directly coupled to IL-6 production via a cAMP/PKA-dependent intracellular pathway.

subject areas

  • Animals
  • Brain
  • Cell Line, Transformed
  • Cell Membrane
  • Cyclic AMP Response Element-Binding Protein
  • Cyclic AMP-Dependent Protein Kinases
  • Endothelium, Vascular
  • Histocompatibility Antigens Class II
  • Interleukin-6
  • Ligands
  • Phosphorylation
  • Protein Kinase C
  • RNA, Messenger
  • Rats
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 10490957
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Additional Document Info

start page

  • 3636

end page

  • 3641

volume

  • 163

issue

  • 7

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