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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1-2
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pubmed:dateCreated |
2007-5-28
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pubmed:abstractText |
The role of tumor necrosis factor (TNF)-alpha and its receptors in the pathogenesis of experimental autoimmune neuritis (EAN) induced by P0 peptide 180-199 in TNFR1 (p55) deficient (TNFR1-/-) mice was investigated. Compared to wild type EAN mice, TNFR1-/- EAN mice developed significantly more severe clinical signs, in parallel with enhanced numbers of inflammatory infiltrating cells in peripheral nerves and splenic P0-reactive T cell proliferation, as well as increased obviously MHC class II and CCR3 expression on the macrophages in the cauda equina. Our data indicated that TNF-alpha might have anti-inflammatory effect preventing the development of EAN in this mouse model.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Ccr3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Myelin P0 Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR3,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Thymidine
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0165-5728
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
186
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
19-26
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17428547-Animals,
pubmed-meshheading:17428547-Cell Proliferation,
pubmed-meshheading:17428547-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:17428547-Flow Cytometry,
pubmed-meshheading:17428547-Histocompatibility Antigens Class II,
pubmed-meshheading:17428547-Immunization,
pubmed-meshheading:17428547-Interferon-gamma,
pubmed-meshheading:17428547-Interleukin-4,
pubmed-meshheading:17428547-Leukocytes, Mononuclear,
pubmed-meshheading:17428547-Mice,
pubmed-meshheading:17428547-Mice, Inbred C57BL,
pubmed-meshheading:17428547-Mice, Knockout,
pubmed-meshheading:17428547-Myelin P0 Protein,
pubmed-meshheading:17428547-Neuritis, Autoimmune, Experimental,
pubmed-meshheading:17428547-Receptors, CCR3,
pubmed-meshheading:17428547-Receptors, Chemokine,
pubmed-meshheading:17428547-Receptors, Tumor Necrosis Factor, Type I,
pubmed-meshheading:17428547-Schwann Cells,
pubmed-meshheading:17428547-Severity of Illness Index,
pubmed-meshheading:17428547-Thymidine
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pubmed:year |
2007
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pubmed:articleTitle |
Aggravation of experimental autoimmune neuritis in TNF-alpha receptor 1 deficient mice.
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pubmed:affiliation |
Division of Neurodegeneration and Neuroinflammation, Karolinska Institute, Karolinska University Hospital Huddinge, Stockholm, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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