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.

Surface Antigen Changes during Normal Neutrophilic Development: A Critical Review

“…However, differentiation beyond the promyelocyte stage is associated with very weak to absent expression (83,84). In vitro activation of granulocytes or administration of G-CSF to healthy individuals is associated with significantly enhanced expression on neutrophils (84,85). DG separation has no effect on CD54 expression on neutrophils (7).…”

Lymphocyte subsets and adhesion molecules expression in heatstroke and heat stress

“…The observed decrease in CD11c ϩ and CD44 ϩ , and to a lesser extent in CD11a ϩ lymphocyte, may contribute to the increased susceptibility to infection reported in heatstroke (3). On the other hand, the increase in CD54 ϩ lymphocytes suggests a state of lymphocyte activation (8) and may play a role in endothelial cell activation and/or injury in heatstroke (5,6).…”

Effects of Escherichia coli and E. coli lipopolysaccharides on the function of human ureteral epithelial cells cultured in serum-free medium

“…I postulated that LPS may have a similar effect on Na+ content in UT cells and that this increase (or changes in ionic gradients coupled to it, e.g., pH and Ca2") may serve as a signal that affects the expression of a member of the immunoglobulin superfamily, ICAM-1, on the surface of UT cells. ICAM-1 is expressed in a variety of cells (2,3,9,15,20,22,23,40) and has been shown to regulate LFA-1-mediated leukocyte adhesion to target cells when rapid and effective yet controlled responses to immune or inflammatory stimuli are required (7,10). Treatment of rapidly proliferating UT cells with LPS resulted in a transient increase in the cellular Na+ content, which is consistent with the possibility that Na+/H+ ex- change was being activated in UT cells.…”

“…By increasing the avidity of this interaction (28), ICAM-1 may play an important role in the interaction of UT cells with lymphocytes during the inflammatory response. ICAM-1 is widely represented on various tissues, including bone marrow-derived cells (2,3), vascular endothelium (9,20), fibroblasts, and some epithelial cells (8), e.g., intestinal (23), renal tubular (22), thymic epithelial (40), and retinal pigment epithelial (15) cells. Constitutive expression varies with the cells examined, but activation studies on humans with interleukin-1, gamma interferon, and tumor necrosis factor alpha indicate that these cytokines can induce ICAM-1 expression considerably (30).…”