PD-L1 (B7-H1) regulation in zones of axonal degeneration

Standard

PD-L1 (B7-H1) regulation in zones of axonal degeneration. / Lipp, Michael; Brandt, Christine; Dehghani, Faramarz; Kwidzinski, Erik; Bechmann, Ingo.

In: NEUROSCI LETT, Vol. 425, No. 3, 02.10.2007, p. 156-61.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Lipp, M, Brandt, C, Dehghani, F, Kwidzinski, E & Bechmann, I 2007, 'PD-L1 (B7-H1) regulation in zones of axonal degeneration', NEUROSCI LETT, vol. 425, no. 3, pp. 156-61. https://doi.org/10.1016/j.neulet.2007.07.053

APA

Lipp, M., Brandt, C., Dehghani, F., Kwidzinski, E., & Bechmann, I. (2007). PD-L1 (B7-H1) regulation in zones of axonal degeneration. NEUROSCI LETT, 425(3), 156-61. https://doi.org/10.1016/j.neulet.2007.07.053

Vancouver

Lipp M, Brandt C, Dehghani F, Kwidzinski E, Bechmann I. PD-L1 (B7-H1) regulation in zones of axonal degeneration. NEUROSCI LETT. 2007 Oct 2;425(3):156-61. https://doi.org/10.1016/j.neulet.2007.07.053

Bibtex

@article{51a0d0e70bb040ec9ff1ae20dd16a068,
title = "PD-L1 (B7-H1) regulation in zones of axonal degeneration",
abstract = "Fibre tract injury evokes recruitment of antigen-presenting- and T cells, but does not cause autoimmune demyelination. This implies that immune tolerance to myelin is actively maintained or readily re-established. Using entorhinal cortex lesion (ECL) to induce axonal degeneration in the hippocampus of adult mice, we studied the induction of B7-H1 (PD-L1) in zones of axonal degeneration. This member of the B7-family has been shown to be expressed on parenchymal cells of various organs, where it strongly down-modulates the activity of T cells. Real-time reverse transcriptase (RT)-PCR revealed low mRNA levels in brain compared to lung and spleen under normal conditions. After ECL, a twofold increase could be observed. Immunocytochemistry revealed astrocytes as source of B7-H1, while immune positive microglia were not detected. Thus, axonal degeneration induces astrocytes to express B7-H1, a potent inhibitor of effector T cells.",
keywords = "Animals, Antigen-Presenting Cells, Antigens, Surface, Apoptosis Regulatory Proteins, Astrocytes, Autoimmunity, Axons, B7-1 Antigen, B7-H1 Antigen, Brain Injuries, Demyelinating Autoimmune Diseases, CNS, Encephalitis, Entorhinal Cortex, Female, Glial Fibrillary Acidic Protein, Gliosis, Immune Tolerance, Lymphocyte Activation, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Peptides, T-Lymphocytes, Wallerian Degeneration, Journal Article, Research Support, Non-U.S. Gov't",
author = "Michael Lipp and Christine Brandt and Faramarz Dehghani and Erik Kwidzinski and Ingo Bechmann",
year = "2007",
month = oct,
day = "2",
doi = "10.1016/j.neulet.2007.07.053",
language = "English",
volume = "425",
pages = "156--61",
journal = "NEUROSCI LETT",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "3",

}

RIS

TY - JOUR

T1 - PD-L1 (B7-H1) regulation in zones of axonal degeneration

AU - Lipp, Michael

AU - Brandt, Christine

AU - Dehghani, Faramarz

AU - Kwidzinski, Erik

AU - Bechmann, Ingo

PY - 2007/10/2

Y1 - 2007/10/2

N2 - Fibre tract injury evokes recruitment of antigen-presenting- and T cells, but does not cause autoimmune demyelination. This implies that immune tolerance to myelin is actively maintained or readily re-established. Using entorhinal cortex lesion (ECL) to induce axonal degeneration in the hippocampus of adult mice, we studied the induction of B7-H1 (PD-L1) in zones of axonal degeneration. This member of the B7-family has been shown to be expressed on parenchymal cells of various organs, where it strongly down-modulates the activity of T cells. Real-time reverse transcriptase (RT)-PCR revealed low mRNA levels in brain compared to lung and spleen under normal conditions. After ECL, a twofold increase could be observed. Immunocytochemistry revealed astrocytes as source of B7-H1, while immune positive microglia were not detected. Thus, axonal degeneration induces astrocytes to express B7-H1, a potent inhibitor of effector T cells.

AB - Fibre tract injury evokes recruitment of antigen-presenting- and T cells, but does not cause autoimmune demyelination. This implies that immune tolerance to myelin is actively maintained or readily re-established. Using entorhinal cortex lesion (ECL) to induce axonal degeneration in the hippocampus of adult mice, we studied the induction of B7-H1 (PD-L1) in zones of axonal degeneration. This member of the B7-family has been shown to be expressed on parenchymal cells of various organs, where it strongly down-modulates the activity of T cells. Real-time reverse transcriptase (RT)-PCR revealed low mRNA levels in brain compared to lung and spleen under normal conditions. After ECL, a twofold increase could be observed. Immunocytochemistry revealed astrocytes as source of B7-H1, while immune positive microglia were not detected. Thus, axonal degeneration induces astrocytes to express B7-H1, a potent inhibitor of effector T cells.

KW - Animals

KW - Antigen-Presenting Cells

KW - Antigens, Surface

KW - Apoptosis Regulatory Proteins

KW - Astrocytes

KW - Autoimmunity

KW - Axons

KW - B7-1 Antigen

KW - B7-H1 Antigen

KW - Brain Injuries

KW - Demyelinating Autoimmune Diseases, CNS

KW - Encephalitis

KW - Entorhinal Cortex

KW - Female

KW - Glial Fibrillary Acidic Protein

KW - Gliosis

KW - Immune Tolerance

KW - Lymphocyte Activation

KW - Membrane Glycoproteins

KW - Mice

KW - Mice, Inbred C57BL

KW - Peptides

KW - T-Lymphocytes

KW - Wallerian Degeneration

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.neulet.2007.07.053

DO - 10.1016/j.neulet.2007.07.053

M3 - SCORING: Journal article

C2 - 17825988

VL - 425

SP - 156

EP - 161

JO - NEUROSCI LETT

JF - NEUROSCI LETT

SN - 0304-3940

IS - 3

ER -