Source:http://linkedlifedata.com/resource/pubmed/id/16547278
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
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| pubmed:dateCreated |
2006-3-20
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| pubmed:abstractText |
Experimental autoimmune encephalomyelitis (EAE) is a CD4(+) Th1 T cell-mediated disease of the CNS, used to study certain aspects of multiple sclerosis. CXCR3, the receptor for CXCL10, CXCL9, and CXCL11, is preferentially expressed on activated Th1 T cells and has been proposed to govern the migration of lymphocytes into the inflamed CNS during multiple sclerosis and EAE. Unexpectedly, CXCL10-deficient mice were susceptible to EAE, leaving uncertain what the role of CXCR3 and its ligands might play in this disease model. In this study, we report that CXCR3(-/-) mice exhibit exaggerated severity of EAE compared with wild-type (CXCR3(+/+)) littermate mice. Surprisingly, there were neither quantitative nor qualitative differences in CNS-infiltrating leukocytes between CXCR3(+/+) and CXCR3(-/-) mice with EAE. Despite these equivalent inflammatory infiltrates, CNS tissues from CXCR3(-/-) mice with EAE showed worsened blood-brain barrier disruption and more von Willebrand factor-immunoreactive vessels within inflamed spinal cords, as compared with CXCR3(+/+) mice. Spinal cords of CXCR3(-/-) mice with EAE demonstrated decreased levels of IFN-gamma, associated with reduced inducible NO synthase immunoreactivity, and lymph node T cells from CXCR3(-/-) mice primed with MOG(35-55) secreted less IFN-gamma in Ag-driven recall responses than cells from CXCR3(+/+) animals. CXCR3(-/-) lymph node T cells also showed enhanced Ag-driven proliferation, which was reduced by addition of IFN-gamma. Taken with prior findings, our data show that CXCL10 is the most relevant ligand for CXCR3 in EAE. CXCR3 does not govern leukocyte trafficking in EAE but modulates T cell IFN-gamma production and downstream events that affect disease severity.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Cxcr3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Myelin Proteolipid Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CXCR3,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine,
http://linkedlifedata.com/resource/pubmed/chemical/myelin oligodendrocyte...,
http://linkedlifedata.com/resource/pubmed/chemical/myelin proteolipid protein (139-151)
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
176
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
4399-409
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| pubmed:dateRevised |
2011-8-26
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| pubmed:meshHeading |
pubmed-meshheading:16547278-Animals,
pubmed-meshheading:16547278-Antibodies,
pubmed-meshheading:16547278-Blood-Brain Barrier,
pubmed-meshheading:16547278-Cell Proliferation,
pubmed-meshheading:16547278-Chemotaxis, Leukocyte,
pubmed-meshheading:16547278-Disease Progression,
pubmed-meshheading:16547278-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:16547278-Glycoproteins,
pubmed-meshheading:16547278-Interferon-gamma,
pubmed-meshheading:16547278-Mice,
pubmed-meshheading:16547278-Mice, Inbred C57BL,
pubmed-meshheading:16547278-Mice, Knockout,
pubmed-meshheading:16547278-Myelin Proteolipid Protein,
pubmed-meshheading:16547278-Nitric Oxide Synthase Type II,
pubmed-meshheading:16547278-Peptide Fragments,
pubmed-meshheading:16547278-Permeability,
pubmed-meshheading:16547278-Receptors, CXCR3,
pubmed-meshheading:16547278-Receptors, Chemokine,
pubmed-meshheading:16547278-T-Lymphocytes
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| pubmed:year |
2006
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| pubmed:articleTitle |
Severe disease, unaltered leukocyte migration, and reduced IFN-gamma production in CXCR3-/- mice with experimental autoimmune encephalomyelitis.
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| pubmed:affiliation |
Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, OH 44195, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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