PD-L1 (B7-H1) regulation in zones of axonal degeneration
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PD-L1 (B7-H1) regulation in zones of axonal degeneration. / Lipp, Michael; Brandt, Christine; Dehghani, Faramarz; Kwidzinski, Erik; Bechmann, Ingo.
in: NEUROSCI LETT, Jahrgang 425, Nr. 3, 02.10.2007, S. 156-61.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -