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

The effects of thymocyte interaction modulation factor on the adhesion of mouse allogeneic thymocytes and B-cells are reported. This glycoprotein, produced by short term cultures of thymocytes, has already been described as reducing the adhesion of syngeneic B-cells, leucocytes and macrophages. Adhesion was measured in suspension culture using the collision efficiency method. This paper reports that: 1. In addition to the syngeneic effect of thymocyte IMF in reducing adhesion of certain unlike cell types there is also an allogeneic effect in which an allogeneic T-IMF will diminish the adhesion of a thymocyte population, or still further reduce the adhesion of a B-cell population than would a syngeneic T-IMF. 2. Thymocyte IMFs were prepared from different congenic strains and tested on the adhesion of syngeneic and allogeneic thymocytes. When factor and cells were syngeneic or matched at any H-2 locus except H-2 D there was no effect on adhesion since it remained at the same value as in controls in their own IMF. But whenever factor and cells were mismatched at H-2 D there was a marked diminution in the adhesion of the cells. 3. Antibodies raised against specific thymocyte IMFs could be used to detect the presence of T-IMF binding to the surface of cells by immunofluorescence or immune cytolysis. These systems show that the antibodies against thymocyte IMF can be used to type the H-2 D type of a cell and that these factors are present at the surface of thymocytes and certain other cell types. They confirm that the thymocyte IMF is either in H-2 D product or is closely associated with H-2 D locus in its binding and action. They also show that the T-IMF antigen on non-lymphocytic types is produced by T-cells or thymocytes. 4. The general relevance of these results is discussed in relation to cell recognition phenomena.
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PMID:The H-2 histocompatibility system and lymphocyte adhesion: interaction modulation factor involvement. 38 48

The regulation of CD11b/CD18 adhesive and phagocytic functions on human polymorphonuclear leukocytes (PMN) in response to LPS was examined. Adhesion of PMN to surfaces coated with LPS had little or no effect on the cells, but pretreating the LPS-coated surfaces with either diluted serum or LPS-binding protein strongly enhanced their ability to bind C3bi-coated E (EC3bi), a ligand for CD11b/CD18. LPS-binding protein is known to enable responses of cells to LPS by facilitating binding of LPS to CD14. Consistent with this, we found that preformed complexes of LPS with soluble rCD14 stimulated binding of ligand by CD11b/CD18 in a concentration-dependent manner. Known agonists that stimulate CD11b/CD18 binding activity on PMN all cause simultaneous enhancement of Fc-mediated phagocytosis. However, LPS presented in complex with either serum proteins or CD14 failed to stimulate the ingestion of ElgG by PMN. The number of FcRs and their ability to bind ligand were not affected by treatment with LPS, nor were they compromised in their ability to respond to other agonists. These results suggest that LPS generates intracellular signals that alter the ability of CD11b/CD18 to bind ligand, but this alteration is not sufficient to promote phagocytosis of IgG-coated particle. This conclusion was confirmed by showing that PMN treated with LPS and serum produced a lipid with the properties of integrin-modulating factor 1: acetone extracts of these cells stimulated CD11b/CD18 adhesive capacity on PMN. However, the lipid did not enhance Fc-mediated phagocytosis. These studies suggest that CD14 affects CD11b/CD18 function by inducing the synthesis of a lipid such as IMF-1, and that this lipid affects only the binding activity, not the phagocytosis-promoting capacity of CD11b/CD18.
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PMID:Different signaling pathways for CD18-mediated adhesion and Fc-mediated phagocytosis. Response of neutrophils to LPS. 751 40