title: Regulation of expression of a human intercellular adhesion molecule (ICAM-1) during lymphohematopoietic differentiation.
abstract: 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.
authors: Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
authors: A W
authors: AW
authors: Boyd
authors: S M
authors: SM
authors: Dunn
authors: J V
authors: JV
authors: Fecondo
authors: J G
authors: JG
authors: Culvenor
authors: U
authors: U
authors: Dührsen
authors: G F
authors: GF
authors: Burns
authors: S O
authors: SO
authors: Wawryk
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal; D000954:Antigens, Surface / Q000032:analysis*; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules; D002449:Cell Aggregation; D002454:Cell Differentiation; D002460:Cell Line; D006410:Hematopoiesis; D006801:Humans; D008214:Lymphocytes / Q000032:analysis / Q000502:physiology* / Q000648:ultrastructure; D008221:Lymphoid Tissue / Q000032:analysis; D008562:Membrane Glycoproteins / Q000032:analysis* / Q000648:ultrastructure; D051379:Mice; D013194:Staining and Labeling; D014407:Tumor Cells, Cultured / Q000032:analysis
chemical_list: D000911:Antibodies, Monoclonal; D000954:Antigens, Surface; D015815:Cell Adhesion Molecules; D008562:Membrane Glycoproteins