Brain endothelial PPARγ controls inflammation-induced CD4+ T cell adhesion and transmigration in vitro

Luisa Klotz, Linda Diehl, Indra Dani, Harald Neumann, Nanette von Oppen, Andreas Dolf, Elmar Endl, Thomas Klockgether, Britta Engelhardt, Percy Knolle

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

An important step in the pathogenesis of multiple sclerosis is adhesion and transmigration of encephalitogenic T cells across brain endothelial cells (EC) which strongly relies on interaction with EC-expressed adhesion molecules. We provide molecular evidence that the transcription factor peroxisome proliferator-activated receptor gamma (PPARγ) is a negative regulator of brain EC inflammation. The PPARγ agonist pioglitazone reduces transendothelial migration of encephalitogenic T cells across TNFα-stimulated brain EC. This effect is clearly PPARγ mediated, as lentiviral PPARγ overexpression in brain EC results in selective abrogation of inflammation-induced ICAM-1 and VCAM-1 upregulation and subsequent adhesion and transmigration of T cells. We therefore propose that PPARγ in brain EC may be exploited to target detrimental EC-T cell interactions under inflammatory conditions.

Original languageEnglish
Pages (from-to)34-43
Number of pages10
JournalJournal of Neuroimmunology
Volume190
Issue number1-2
DOIs
StatePublished - Oct 2007
Externally publishedYes

Keywords

  • Adhesion
  • Endothelial cells
  • Transcription factor
  • Transmigration

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