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

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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, Jahrgang 190, Nr. 1-2, 10.2007, S. 34-43.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Klotz, L, Diehl, L, Dani, I, Neumann, H, von Oppen, N, Dolf, A, Endl, E, Klockgether, T, Engelhardt, B & Knolle, P 2007, 'Brain endothelial PPARgamma controls inflammation-induced CD4+ T cell adhesion and transmigration in vitro', J NEUROIMMUNOL, Jg. 190, Nr. 1-2, S. 34-43. https://doi.org/10.1016/j.jneuroim.2007.07.017

APA

Klotz, L., Diehl, L., Dani, I., Neumann, H., von Oppen, N., Dolf, A., Endl, E., Klockgether, T., Engelhardt, B., & Knolle, P. (2007). Brain endothelial PPARgamma controls inflammation-induced CD4+ T cell adhesion and transmigration in vitro. J NEUROIMMUNOL, 190(1-2), 34-43. https://doi.org/10.1016/j.jneuroim.2007.07.017

Vancouver

Bibtex

@article{8475bb0b1ada489eba9bb683dd569c1a,
title = "Brain endothelial PPARgamma controls inflammation-induced CD4+ T cell adhesion and transmigration in vitro",
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 (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.",
keywords = "Animals, Brain, CD4-Positive T-Lymphocytes, Cell Adhesion, Cell Line, Cerebral Arteries, Chemotaxis, Leukocyte, Encephalitis, Endothelial Cells, Gene Expression, Genetic Vectors, Hypoglycemic Agents, Intercellular Adhesion Molecule-1, Lentivirus, Mice, Mice, Inbred BALB C, PPAR gamma, Thiazolidinediones, Tumor Necrosis Factor-alpha, Vascular Cell Adhesion Molecule-1",
author = "Luisa Klotz and Linda Diehl and Indra Dani and Harald Neumann and {von Oppen}, Nanette and Andreas Dolf and Elmar Endl and Thomas Klockgether and Britta Engelhardt and Percy Knolle",
year = "2007",
month = oct,
doi = "10.1016/j.jneuroim.2007.07.017",
language = "English",
volume = "190",
pages = "34--43",
journal = "J NEUROIMMUNOL",
issn = "0165-5728",
publisher = "Elsevier",
number = "1-2",

}

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 -