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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2010-7-5
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pubmed:abstractText |
Innate glial response is critical for the induction of inflammatory mediators and recruitment of leukocytes to sites of the injury in the CNS. We have examined the involvement of type I IFN signaling in the mouse hippocampus following sterile injury (transection of entorhinal afferents). Type I IFNs signal through a receptor (IFNAR), which involves activation of IFN regulatory factor (IRF)9, leading to the induction of IFN-stimulated genes including IRF7, that in turn enhances the induction of type I IFN. Axonal transection induced upregulation of IRF7 and IRF9 in hippocampus. Induction of IRF7 and IRF9 mRNAs was IFNAR dependent. Double-labeling immunofluorescence showed that IRF7 selectively was induced in Mac-1/CD11b(+) macrophages/microglia in hippocampus after axonal transection. IRF7 mRNA was also detected in microglia sorted by flow cytometry. Lack of type I IFN signaling resulted in increased leukocyte infiltration into the lesion-reactive hippocampus. Axonal lesion-induced CXCL10 gene expression was abrogated, whereas matrix metalloproteinase 9 mRNA was elevated in IFNAR-deficient mice. Our findings point to a role for type I IFN signaling in regulation of CNS response to sterile injury.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD11b,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL10,
http://linkedlifedata.com/resource/pubmed/chemical/Cxcl10 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Glial Fibrillary Acidic Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Regulatory Factor-7,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Irf7 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinase 9,
http://linkedlifedata.com/resource/pubmed/chemical/Mmp9 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Interferon alpha-beta,
http://linkedlifedata.com/resource/pubmed/chemical/STAT1 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Stat1 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1550-6606
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
185
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1258-64
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pubmed:meshHeading |
pubmed-meshheading:20562259-Animals,
pubmed-meshheading:20562259-Antigens, CD11b,
pubmed-meshheading:20562259-Blotting, Western,
pubmed-meshheading:20562259-Brain Injuries,
pubmed-meshheading:20562259-Central Nervous System,
pubmed-meshheading:20562259-Chemokine CXCL10,
pubmed-meshheading:20562259-Female,
pubmed-meshheading:20562259-Glial Fibrillary Acidic Protein,
pubmed-meshheading:20562259-Hippocampus,
pubmed-meshheading:20562259-Immunohistochemistry,
pubmed-meshheading:20562259-Inflammation,
pubmed-meshheading:20562259-Inflammation Mediators,
pubmed-meshheading:20562259-Interferon Regulatory Factor-7,
pubmed-meshheading:20562259-Interferon Type I,
pubmed-meshheading:20562259-Leukocytes,
pubmed-meshheading:20562259-Matrix Metalloproteinase 9,
pubmed-meshheading:20562259-Mice,
pubmed-meshheading:20562259-Mice, Inbred C57BL,
pubmed-meshheading:20562259-Mice, Inbred Strains,
pubmed-meshheading:20562259-Mice, Knockout,
pubmed-meshheading:20562259-Receptor, Interferon alpha-beta,
pubmed-meshheading:20562259-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:20562259-STAT1 Transcription Factor,
pubmed-meshheading:20562259-Signal Transduction
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pubmed:year |
2010
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pubmed:articleTitle |
Injury-induced type I IFN signaling regulates inflammatory responses in the central nervous system.
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pubmed:affiliation |
Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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