Source:http://linkedlifedata.com/resource/pubmed/id/11431002
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-2
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pubmed:dateCreated |
2001-6-29
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pubmed:abstractText |
Recent evidence suggests that T-lymphocyte extravasation and CNS-parenchymal infiltration during autoimmune disease might be regulated by antigen-presenting (ED2(+)) cerebral/spinal perivascular phagocytes (CPP/SPP). Since the massive erythrocytic and leukocytic infiltrates in the CNS of rats with experimental allergic encephalomyelitis do not allow a precise differentiation between CPP/SPP and the invading cells in the Virchow-Robin space, we developed a new immune-response model whereby the extravasation of T-lymphocytes was not followed by other blood cells. Adult Lewis rats were sensitized to horseradish peroxidase (HRP). Subsequent intracerebroventricular (i.c.v.) injections of HRP and/or Fluoro-Emerald (FE) served to: (1) challenge the primed T-lymphocytes and (2) label the CPP/SPP for additional immunocytochemical analysis. We found that 24 h and 3 days after single, double, or triple antigen boosting T-lymphocytes (R73(+), W3/25(+), OX50(+)) entered the Virchow-Robin space but did not break through the astrocytic glia limitans. Instead they adhered to HRP-containing activated CPP/SPP (mabs OX-6(+), SILK6(+), CD40(+), CD80(+), CD86(+)). This selective contact was mediated neither by cell adhesion molecules (P-selectin, ICAM-1, VCAM-1), nor promoted by chemokine receptors (CCR1, CCR5) or chemokines (monocyte chemoattractant protein (MCP)-1, MIP-1alpha, MIP-1beta, RANTES). This non-inflammatory, but antigen-dependent lymphocyte extravasation provides optimal conditions to further study the CNS immune response.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Ccr1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL3,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL4,
http://linkedlifedata.com/resource/pubmed/chemical/Horseradish Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Macrophage Inflammatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, CCR1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0165-5728
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
2
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pubmed:volume |
117
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
30-42
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11431002-Animals,
pubmed-meshheading:11431002-Blood-Brain Barrier,
pubmed-meshheading:11431002-Brain,
pubmed-meshheading:11431002-Cell Adhesion,
pubmed-meshheading:11431002-Chemokine CCL3,
pubmed-meshheading:11431002-Chemokine CCL4,
pubmed-meshheading:11431002-Horseradish Peroxidase,
pubmed-meshheading:11431002-Intercellular Adhesion Molecule-1,
pubmed-meshheading:11431002-Lymphocytes,
pubmed-meshheading:11431002-Macrophage Inflammatory Proteins,
pubmed-meshheading:11431002-Male,
pubmed-meshheading:11431002-Phagocytes,
pubmed-meshheading:11431002-Rats,
pubmed-meshheading:11431002-Rats, Inbred Lew,
pubmed-meshheading:11431002-Receptors, CCR1,
pubmed-meshheading:11431002-Receptors, Chemokine,
pubmed-meshheading:11431002-Vascular Cell Adhesion Molecule-1
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pubmed:year |
2001
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pubmed:articleTitle |
Exogenous antigen containing perivascular phagocytes induce a non-encephalitogenic extravasation of primed lymphocytes.
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pubmed:affiliation |
Institut I für Anatomie der Universität zu Köln, Joseph-Stelzmann-Strasse 9, D-50931, Cologne, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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