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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1997-8-5
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pubmed:abstractText |
The objective of this research was to investigate the cellular source of soluble ICAM-1 (siCAM-1) from rheumatoid synovial tissue (RS) and its relation to sICAM-1 in synovial fluid (SF) and serum, and to study the expression of ICAM-1 in isolated cells of RS. sICAM-1 was determined by using the enzyme-linked immunosorbent assay (ELISA) and Western blot analysis in supernatants from RS cultured for short periods (n = 19), in SF (n = 7) and in serum (n = 19). ICAM-1 expression, vascularization and inflammatory infiltration (CD3, CD68, CD22) were characterized immunohistochemically in cytospin preparations (n = 18), cryosections (n = 18) and in conventionally stained paraffin sections (n = 19) of RS. The degree of RS vascularization was analysed morphometrically in immunohistochemically stained cryosections (factor VIII related antigen). We found 90-kD sICAM-1 in supernatants of cultured cells, in SF and in sera. sICAM-1 in cellular supernatant correlated significantly (P < 0.01) with SF sICAM-1. The amount of sICAM in cellular supernatants showed no correlation to the score of inflammatory infiltration, but correlated significantly (P < 0.001) with the vascularization index of RS. The percentage of ICAM-1-expressing cells correlated significantly (P < 0.001) with the percentage of CD68-positive macrophages, but not with CD3- and CD22-positive lymphocytes. Macrophages, multinucleated giant cells and endothelial cells exhibited a higher expression of ICAM-1 as compared to lymphocytes and fibroblasts. The differential expression of ICAM-1 on infiltrating leucocytes and resident cells of RS indicates a functional role of ICAM-1 in the local inflammatory process. SF sICAM-1 originated in RS, but serum sICAM-1 did not. Shedding of sICAM-1 by RS was independent of inflammatory infiltration, but depended on the degree of vascularization, indicating that endothelial cells are the major source of sICAM-1 in RS.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0172-8172
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
17
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
17-27
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:9194210-Adult,
pubmed-meshheading:9194210-Aged,
pubmed-meshheading:9194210-Aged, 80 and over,
pubmed-meshheading:9194210-Arthritis, Rheumatoid,
pubmed-meshheading:9194210-Blotting, Western,
pubmed-meshheading:9194210-Cells, Cultured,
pubmed-meshheading:9194210-Endothelium,
pubmed-meshheading:9194210-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:9194210-Female,
pubmed-meshheading:9194210-Humans,
pubmed-meshheading:9194210-Immunohistochemistry,
pubmed-meshheading:9194210-Intercellular Adhesion Molecule-1,
pubmed-meshheading:9194210-Male,
pubmed-meshheading:9194210-Middle Aged,
pubmed-meshheading:9194210-Synovial Membrane
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pubmed:year |
1997
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pubmed:articleTitle |
Endothelial cells are the major source of sICAM-1 in rheumatoid synovial tissue.
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pubmed:affiliation |
Institute of Pathology, University of Würzburg, Germany.
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pubmed:publicationType |
Journal Article
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