ICAM-1 a ligand for LFA-1-dependent adhesion of B, T and myeloid cells

Abstract

Cell-cell adhesion is essential for many immunological functions. The LFA-1 molecule, a member of a superfamily of adhesion molecules, participates in adhesion which is critical to the function of each of the three major subsets of leukocytes: lymphocytes, monocytes and granulocytes. Putative LFA-1 ligands have been identified functionally in different laboratories using three different monoclonal antibodies that inhibit LFA-1-mediated leukocyte adhesion in particular model systems; however, there may be more than one LFA-1 ligand. We have directly compared the three relevant monoclonal antibodies, and show that each binds to the same molecule, intercellular-adhesion molecule-1 (ICAM-1). Most important, B, T and myeloid cells adhere specifically to purified ICAM-1-coated surfaces; such adhesion has distinctive requirements for Mg2+ and Ca2+. This constitutes biochemical evidence that ICAM-1 functions as a ligand for LFA-1-dependent adhesion by a variety of leukocytes.

Modulation of Expression of Endothelial Intercellular Adhesion Molecule-1, Platelet–Endothelial Cell Adhesion Molecule-1, and Vascular Cell Adhesion Molecule-1 in Aortic Arch Lesions of Apolipoprotein E–Deficient Compared With Wild-Type Mice

“…23,24 Among a number of adhesion molecules implicated in the homing of leukocytes to sites of inflammation, endothelial ICAM-1 and its leukocyte ligand CD11a/CD18 (also known as ␣ L ␤ 2 or lymphocyte function-associated antigen-1) play a major role in this process. 25,26 In the present study, a significant modulation of ICAM-1 expression over time by endothelial cells lining the whole vessel wall circumference was observed for the aortic arch region of apoE-deficient mice fed a fat or chow diet. Northern blots on aortic arch samples, for determination of ICAM-1 gene expression, showed an increase at 6 weeks (by at least 2-fold) compared with 0 and 16 weeks in C57BL6 and apoE animals.…”

Increased serum levels of circulating intercellular adhesion molecule 1 predict the risk of graft rejection after bone marrow transplantation for thalassemia

“…4 One adhesion pathway in man involves the ␤2 leukocyte cantly increased levels of sICAM-1 were found in the patients who subsequently rejected the graft (mean integrin LFA-1 (CD11a/CD18) and its ligand, the intercellular adhesion molecule 1 (ICAM-1/CD54). 5,6 The (95% CI) = 490 ng/ml (440; 540) ) as compared to those with sustained engraftment (400 ng/ml (384; 415) ), (P ICAM-1 molecule is a single chain glycoprotein of 90 kDa, composed of five Ig-like extracellular domains, a hydro-= 0.004). The mean level of sICAM-1 in patients with early rejection was significantly higher than that in phobic transmembrane domain and a short cytoplasmic domain.…”

ICAM-1 Deficiency Reduces Atherosclerotic Lesions in Double-Knockout Mice (ApoE − /− /ICAM-1 − /− ) Fed a Fat or a Chow Diet

“…19 Among a number of adhesion molecules implicated in the homing of leukocytes to sites of inflammation, endothelial ICAM-1 and its leukocyte ligand CD11a/CD18 (also known as ␣ L ␤ 2 or LFA-1) play a major role in this process. 36,37 Monocytes attracted by endothelial released MCP-1 can bind directly through CD11a/CD18 to vascular ICAM-1 and/or by fibrinogen through CD11b/CD18 (also known as ␣ M ␤ 2 or MAC-1) and ICAM-1. 38 Constitutive levels of ICAM-1 in mice differ markedly from one organ to another.…”