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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
1996-11-19
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pubmed:abstractText |
To identify potential molecular substrates for leukocyte trafficking and activation in multiple sclerosis (MS) brain, we determined the immunocytochemical distribution of the beta, integrin lymphocyte-function-associated antigen-1 (LFA-1) and its major ligands, intercellular adhesion molecule (ICAM)-1, ICAM-2, and ICAM-3 in MS tissue. Colocalization of these adhesion molecules with lineage-specific markers was analyzed by dual-labeling immunocytochemistry and confocal microscopy. ICAM-1 and ICAM-2 were detected on endothelial cells, and ICAM-3 immunoreactivity was restricted to infiltrating leukocytes. In control brain, 10% of glucose transporter-1 positive vessels contained ICAM-1 immunoreactivity on their luminal surface and 21% were ICAM-2-positive. A significant increase in ICAM-1-positive vessels was found in MS brains. This increase was greater in MS lesions (81% of vessels) than in nonlesion areas (37% of vessels). A significant increase in ICAM-1-positive vessels was found in encephalitis (55% of vessels) but not in Parkinson's (17% of vessels) brains. The percentage of vessels expressing ICAM-2 was not increased in MS, encephalitis, or Parkinson's brains. Both ICAM-3 and LFA-1 were detected on the vast majority of infiltrating lymphocytes and monocytes in and near MS lesions, and these cells were often closely apposed to each other. In addition, LFA-1 was detected on activated microglia located close to the edge of demyelinating lesions. ICAM-3-positive leukocytes were often closely apposed to LFA-1-positive microglia. These results suggest a role for ICAM-1, -2, and LFA-1 in the transendothelial migration of leukocytes into MS brain and a role for ICAM 3/LFA-1 interactions in the activation of lymphocytes, monocytes, and microglia in MS lesions.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/ICAM2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/ICAM3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphocyte Function-Associated...
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-3069
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
55
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1060-72
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pubmed:dateRevised |
2008-6-13
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pubmed:meshHeading |
pubmed-meshheading:8858003-Adolescent,
pubmed-meshheading:8858003-Adult,
pubmed-meshheading:8858003-Aged,
pubmed-meshheading:8858003-Aged, 80 and over,
pubmed-meshheading:8858003-Antigens, CD,
pubmed-meshheading:8858003-Antigens, Differentiation,
pubmed-meshheading:8858003-Brain,
pubmed-meshheading:8858003-Brain Chemistry,
pubmed-meshheading:8858003-Cell Adhesion Molecules,
pubmed-meshheading:8858003-Child,
pubmed-meshheading:8858003-Child, Preschool,
pubmed-meshheading:8858003-Endothelium,
pubmed-meshheading:8858003-Humans,
pubmed-meshheading:8858003-Infant,
pubmed-meshheading:8858003-Infant, Newborn,
pubmed-meshheading:8858003-Intercellular Adhesion Molecule-1,
pubmed-meshheading:8858003-Leukocytes,
pubmed-meshheading:8858003-Lymphocyte Function-Associated Antigen-1,
pubmed-meshheading:8858003-Microscopy, Confocal,
pubmed-meshheading:8858003-Middle Aged,
pubmed-meshheading:8858003-Multiple Sclerosis
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pubmed:year |
1996
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pubmed:articleTitle |
Distribution of immunoglobulin superfamily members ICAM-1, -2, -3, and the beta 2 integrin LFA-1 in multiple sclerosis lesions.
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pubmed:affiliation |
Department of Neurosciences, Cleveland Clinic Foundation, Ohio 44195, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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