Brain endothelial PPARgamma controls inflammation-induced CD4+ T cell adhesion and transmigration in vitro
Standard
Brain endothelial PPARgamma controls inflammation-induced CD4+ T cell adhesion and transmigration in vitro. / Klotz, Luisa; Diehl, Linda; Dani, Indra; Neumann, Harald; von Oppen, Nanette; Dolf, Andreas; Endl, Elmar; Klockgether, Thomas; Engelhardt, Britta; Knolle, Percy.
In: J NEUROIMMUNOL, Vol. 190, No. 1-2, 10.2007, p. 34-43.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Brain endothelial PPARgamma controls inflammation-induced CD4+ T cell adhesion and transmigration in vitro
AU - Klotz, Luisa
AU - Diehl, Linda
AU - Dani, Indra
AU - Neumann, Harald
AU - von Oppen, Nanette
AU - Dolf, Andreas
AU - Endl, Elmar
AU - Klockgether, Thomas
AU - Engelhardt, Britta
AU - Knolle, Percy
PY - 2007/10
Y1 - 2007/10
N2 - 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 (PPARgamma) is a negative regulator of brain EC inflammation. The PPARgamma agonist pioglitazone reduces transendothelial migration of encephalitogenic T cells across TNFalpha-stimulated brain EC. This effect is clearly PPARgamma mediated, as lentiviral PPARgamma 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 PPARgamma in brain EC may be exploited to target detrimental EC-T cell interactions under inflammatory conditions.
AB - 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 (PPARgamma) is a negative regulator of brain EC inflammation. The PPARgamma agonist pioglitazone reduces transendothelial migration of encephalitogenic T cells across TNFalpha-stimulated brain EC. This effect is clearly PPARgamma mediated, as lentiviral PPARgamma 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 PPARgamma in brain EC may be exploited to target detrimental EC-T cell interactions under inflammatory conditions.
KW - Animals
KW - Brain
KW - CD4-Positive T-Lymphocytes
KW - Cell Adhesion
KW - Cell Line
KW - Cerebral Arteries
KW - Chemotaxis, Leukocyte
KW - Encephalitis
KW - Endothelial Cells
KW - Gene Expression
KW - Genetic Vectors
KW - Hypoglycemic Agents
KW - Intercellular Adhesion Molecule-1
KW - Lentivirus
KW - Mice
KW - Mice, Inbred BALB C
KW - PPAR gamma
KW - Thiazolidinediones
KW - Tumor Necrosis Factor-alpha
KW - Vascular Cell Adhesion Molecule-1
U2 - 10.1016/j.jneuroim.2007.07.017
DO - 10.1016/j.jneuroim.2007.07.017
M3 - SCORING: Journal article
C2 - 17719655
VL - 190
SP - 34
EP - 43
JO - J NEUROIMMUNOL
JF - J NEUROIMMUNOL
SN - 0165-5728
IS - 1-2
ER -