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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
1989-6-16
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pubmed:abstractText |
The intercellular adhesion molecule (ICAM-1) is a cell-surface molecule which binds to leukocyte function antigen-1 (LFA-1) and regulates both leukocyte adhesion to endothelial cells and immune functions requiring cell-cell contact. Membrane expression of ICAM-1 is highly regulated on all hematopoietic lineages. Cell membrane antigen is significantly expressed on a small subset of bone marrow (BM) progenitors but is weak or absent on all cell lineages once they enter the circulation. However, strong expression on tissue macrophages and germinal center B cells suggested that activated cells may show upregulated expression. When B cells, T cells, macrophages, or granulocytes were activated in vitro by suitable mitogens, ICAM-1 expression was induced in all cases. Parallel studies of hematopoietic tumors demonstrated a heterogeneity of expression which correlated with expression on their normal cellular counterparts. In particular, a striking correlation between expression on B-cell tumors and corresponding stages of B-cell differentiation was noted. The widely varying expression of ICAM-1 contrasts with LFA-1 which, while variable, is nevertheless significantly positive at all stages of differentiation. This suggests that the major regulation of homotypic adhesion mediated by the LFA-1/ICAM-1 linkage occurs through control of ICAM-1 expression. In keeping with this notion, ICAM-1 expression was also correlated with the "adhesiveness" of B-lymphoid tumors. Large solitary lymphoma masses showed intense expression of ICAM-1. Conversely, chronic lymphocytic leukemia (CLL) cells and lymphoma cells from tumors exhibiting diffuse, widespread lymph node disease showed weak expression. These observations are discussed in relation to the role of ICAM-1 in regulation of lymphoid recirculation and the biology of lymphoid tumors.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0006-4971
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
|
pubmed:volume |
73
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1896-903
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:2469503-Animals,
pubmed-meshheading:2469503-Antibodies, Monoclonal,
pubmed-meshheading:2469503-Antigens, Surface,
pubmed-meshheading:2469503-Cell Adhesion,
pubmed-meshheading:2469503-Cell Adhesion Molecules,
pubmed-meshheading:2469503-Cell Aggregation,
pubmed-meshheading:2469503-Cell Differentiation,
pubmed-meshheading:2469503-Cell Line,
pubmed-meshheading:2469503-Hematopoiesis,
pubmed-meshheading:2469503-Humans,
pubmed-meshheading:2469503-Lymphocytes,
pubmed-meshheading:2469503-Lymphoid Tissue,
pubmed-meshheading:2469503-Membrane Glycoproteins,
pubmed-meshheading:2469503-Mice,
pubmed-meshheading:2469503-Staining and Labeling,
pubmed-meshheading:2469503-Tumor Cells, Cultured
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pubmed:year |
1989
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pubmed:articleTitle |
Regulation of expression of a human intercellular adhesion molecule (ICAM-1) during lymphohematopoietic differentiation.
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pubmed:affiliation |
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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