Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CD4 is the surface receptor for HIV envelope. Some evidence exists, however, that other cell surface receptors may be involved in viral entry subsequent to the initial binding of gp120 to CD4. Antibodies to leukocyte integrin LFA-1, a major component of intercellular adhesive interactions, have been shown to inhibit HIV-induced syncytia formation. Using a stringent system for in vitro HIV infection of human leukocytes, we examine the ability of some monoclonal antibodies (mAb) against various adhesion-related molecules to block or partially inhibit productive viral replication. HIV-1 infection of target monocytes or T cells by cell-free virus was blocked completely or partially by some mAb that prevent cell-cell interactions (CD4, HLA-DR, LFA-1, LFA-3), but not by others (ICAM-1, MAC-1, gp150.95, CD2, CD3, CD14). The capacity for mAb to block HIV infection appears to be epitope-specific, and does not relate to the ability to block homotypic adhesion. HIV transmission from infected cells was more difficult to block than was infection by cell-free virus. Adhesion molecules may be involved in facilitating early stages of HIV infection, following gp120/CD4 binding but prior to viral integration, in a manner distinct from cell-cell adhesion.
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PMID:Inhibition of human immunodeficiency virus infection in monocytes by monoclonal antibodies against leukocyte adhesion molecules. 175 7

Surface phenotypes and adhesion activity to human umbilical vein endothelial cells (HUVECs) were studied using leukemic cells from 12 Japanese patients with B-cell chronic lymphoid leukemias including 7 with chronic lymphocytic leukemia (CLL), 1 with prolymphocytic leukemia (PLL), 2 with hairy cell leukemia (HCL) and 2 with HCL variant (HCL-V). CD13 and CD23 were found to be characteristically positive in CLL, whereas they were not expressed in non-CLL cases except for positivity of CD23 in two such cases. Except for CD11b, all other leukocyte integrins examined (CD11a, CD11c and CD18) and their ligand (CD54) were highly expressed in non-CLL cases. Adhesion activity of leukemic cells to HUVECs after co-culture with HUVECs was well correlated with the expression of CD11b, CD18 and CD54, but showed no predilection for any leukemia subtype. Positivity for CD5, CD21, CD23 and CD13 changed after the co-culture with HUVEC. These results suggest that adhesion activity after co-culture. does not correlate with the leukemia subtype and that endothelial cells activate or differentiate leukemic cells.
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PMID:Surface phenotype and adhesion activity of B-cell chronic lymphoid leukemias. 822 Jan 19

Aminopeptidase N (APN)/CD13 is a transmembrane ectoenzyme expressed on a wide variety of cells. With respect to haematopoietic cells, APN/CD13 has been considered specific for the myeloid lineage, because granulocytes and monocytes/macrophages, but not lymphocytes of peripheral blood, show a surface expression of CD13 antigen. However, we could recently show that cell-cell contact of lymphocytes with endothelial cells, monocytes, and fibroblast-like synoviocytes (SFCs) results in an increase of steady-state APN/CD13 mRNA and a rapid expression of cell-surface protein on the lymphocytes. In this study using the Dual-Luciferase reporter assay, we demonstrate that interaction of the T-cell line Jurkat with SFCs results in a higher activity of the APN/CD13 myeloid promoter in T cells. An enhancer located between the myeloid and epithelial APN/CD13 promoter increases the response of the promoter to the cell-cell contact-induced expression of APN/CD13 in lymphocytes. Adhesion of lymphocytes to extracellular matrix did not result in increased promoter activity. The lymphocytic promoter response induced by direct cell-cell contact with SFCs is not affected by mutations of a proximal promoter element (nucleotides -48 to -35), which has a possible functional role in the basal APN/CD13 gene expression in lymphocytes. Upregulated peptidase-promoter activity via cell-cell contact shown in this study for the first time is discussed as a general mechanism in peptidase induction.
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PMID:Increased lymphocytic aminopeptidase N/CD13 promoter activity after cell-cell contact. 1102 58