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B7-H1 restricts neuroantigen-specific T cell responses and confines inflammatory CNS damage: implications for the lesion pathogenesis of multiple sclerosis.

Research output: Journal contributions › Journal articles › Research

Standard

B7-H1 restricts neuroantigen-specific T cell responses and confines inflammatory CNS damage: implications for the lesion pathogenesis of multiple sclerosis. / Ortler, Sonja; Leder, Christoph; Mittelbronn, Michel et al.
In: European Journal of Immunology, Vol. 38, No. 6, 06.2008, p. 1734-1744.

Research output: Journal contributions › Journal articles › Research

Harvard

Ortler, S, Leder, C, Mittelbronn, M, Zozulya, AL, Knolle, PA, Kroner, A, Wiendl, H & Chen, L 2008, 'B7-H1 restricts neuroantigen-specific T cell responses and confines inflammatory CNS damage: implications for the lesion pathogenesis of multiple sclerosis.', European Journal of Immunology, vol. 38, no. 6, pp. 1734-1744. https://doi.org/10.1002/eji.200738071

APA

Ortler, S., Leder, C., Mittelbronn, M., Zozulya, A. L., Knolle, P. A., Kroner, A., Wiendl, H., & Chen, L. (2008). B7-H1 restricts neuroantigen-specific T cell responses and confines inflammatory CNS damage: implications for the lesion pathogenesis of multiple sclerosis. European Journal of Immunology, 38(6), 1734-1744. https://doi.org/10.1002/eji.200738071

Vancouver

Ortler S, Leder C, Mittelbronn M, Zozulya AL, Knolle PA, Kroner A et al. B7-H1 restricts neuroantigen-specific T cell responses and confines inflammatory CNS damage: implications for the lesion pathogenesis of multiple sclerosis. European Journal of Immunology. 2008 Jun;38(6):1734-1744. doi: 10.1002/eji.200738071

Bibtex

@article{b8c0f1db499f4cde9edbf2ec662713f5,
title = "B7-H1 restricts neuroantigen-specific T cell responses and confines inflammatory CNS damage: implications for the lesion pathogenesis of multiple sclerosis.",
abstract = "The co-inhibitory B7-homologue 1 (B7-H1/PD-L1) influences adaptive immune responses and has been proposed to contribute to the mechanisms maintaining peripheral tolerance and limiting inflammatory damage in parenchymal organs. To understand the B7-H1/PD1 pathway in CNS inflammation, we analyzed adaptive immune responses in myelin oligodendrocyte glycoprotein (MOG) 35- 55-induced EAE and assessed the expression of B7-H1 in human CNS tissue. B7-H1 -/- mice exhibited an accelerated disease onset and significantly exacerbated EAE severity, although absence of B7-H1 had no influence on MOG antibody production. Peripheral MOG-specific IFN-γ/IL-17 T cell responses occurred earlier and enhanced in B7-H1 -/- mice, but ceased more rapidly. In the CNS, however, significantly higher numbers of activated neuroantigen-specific T cells persisted during all stages of EAE. Experiments showing a direct inhibitory role of APC-derived B7-H1 on the activation of MOG-specific effector cells support the assumption that parenchymal B7-H1 is pivotal for delineating T cell fate in the target organ. Compatible with this concept, our data investigating human brain tissue specimens show a strong up-regulation of B7-H1 in lesions of multiple sclerosis. Our findings demonstrate the critical importance of B7-H1 as an immune-inhibitory molecule capable of down-regulating T cell responses thus contributing to the confinement of immunopathological damage.",
keywords = "Chemistry, Co-stimulation, EAE, Inflammation, MS",
author = "Sonja Ortler and Christoph Leder and Michel Mittelbronn and Zozulya, {Alla L.} and Knolle, {Percy A.} and Antje Kroner and Heinz Wiendl and Lieping Chen",
year = "2008",
month = jun,
doi = "10.1002/eji.200738071",
language = "English",
volume = "38",
pages = "1734--1744",
journal = "European Journal of Immunology",
issn = "0014-2980",
publisher = "Wiley-VCH Verlag",
number = "6",

}

RIS

TY - JOUR

T1 - B7-H1 restricts neuroantigen-specific T cell responses and confines inflammatory CNS damage: implications for the lesion pathogenesis of multiple sclerosis.

AU - Ortler, Sonja

AU - Leder, Christoph

AU - Mittelbronn, Michel

AU - Zozulya, Alla L.

AU - Knolle, Percy A.

AU - Kroner, Antje

AU - Wiendl, Heinz

AU - Chen, Lieping

PY - 2008/6

Y1 - 2008/6

N2 - The co-inhibitory B7-homologue 1 (B7-H1/PD-L1) influences adaptive immune responses and has been proposed to contribute to the mechanisms maintaining peripheral tolerance and limiting inflammatory damage in parenchymal organs. To understand the B7-H1/PD1 pathway in CNS inflammation, we analyzed adaptive immune responses in myelin oligodendrocyte glycoprotein (MOG) 35- 55-induced EAE and assessed the expression of B7-H1 in human CNS tissue. B7-H1 -/- mice exhibited an accelerated disease onset and significantly exacerbated EAE severity, although absence of B7-H1 had no influence on MOG antibody production. Peripheral MOG-specific IFN-γ/IL-17 T cell responses occurred earlier and enhanced in B7-H1 -/- mice, but ceased more rapidly. In the CNS, however, significantly higher numbers of activated neuroantigen-specific T cells persisted during all stages of EAE. Experiments showing a direct inhibitory role of APC-derived B7-H1 on the activation of MOG-specific effector cells support the assumption that parenchymal B7-H1 is pivotal for delineating T cell fate in the target organ. Compatible with this concept, our data investigating human brain tissue specimens show a strong up-regulation of B7-H1 in lesions of multiple sclerosis. Our findings demonstrate the critical importance of B7-H1 as an immune-inhibitory molecule capable of down-regulating T cell responses thus contributing to the confinement of immunopathological damage.

AB - The co-inhibitory B7-homologue 1 (B7-H1/PD-L1) influences adaptive immune responses and has been proposed to contribute to the mechanisms maintaining peripheral tolerance and limiting inflammatory damage in parenchymal organs. To understand the B7-H1/PD1 pathway in CNS inflammation, we analyzed adaptive immune responses in myelin oligodendrocyte glycoprotein (MOG) 35- 55-induced EAE and assessed the expression of B7-H1 in human CNS tissue. B7-H1 -/- mice exhibited an accelerated disease onset and significantly exacerbated EAE severity, although absence of B7-H1 had no influence on MOG antibody production. Peripheral MOG-specific IFN-γ/IL-17 T cell responses occurred earlier and enhanced in B7-H1 -/- mice, but ceased more rapidly. In the CNS, however, significantly higher numbers of activated neuroantigen-specific T cells persisted during all stages of EAE. Experiments showing a direct inhibitory role of APC-derived B7-H1 on the activation of MOG-specific effector cells support the assumption that parenchymal B7-H1 is pivotal for delineating T cell fate in the target organ. Compatible with this concept, our data investigating human brain tissue specimens show a strong up-regulation of B7-H1 in lesions of multiple sclerosis. Our findings demonstrate the critical importance of B7-H1 as an immune-inhibitory molecule capable of down-regulating T cell responses thus contributing to the confinement of immunopathological damage.

KW - Chemistry

KW - Co-stimulation

KW - EAE

KW - Inflammation

KW - MS

UR - http://www.scopus.com/inward/record.url?scp=49649111913&partnerID=8YFLogxK

UR - https://www.mendeley.com/catalogue/e246980c-d867-3c04-96f8-094c430d852a/

U2 - 10.1002/eji.200738071

DO - 10.1002/eji.200738071

M3 - Journal articles

VL - 38

SP - 1734

EP - 1744

JO - European Journal of Immunology

JF - European Journal of Immunology

SN - 0014-2980

IS - 6

ER -

DOI

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