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)

We have studied the role of major histocompatibility complex (MHC) molecules in the regulation of intercellular adhesion of human B cells. We found that molecules able to bind to MHC class II molecules, such as monoclonal antibodies or staphylococcal enterotoxins, induced rapid and sustained homotypic adhesion of Epstein-Barr virus (EBV)-transformed B cell lines as well as peripheral blood B lymphocytes. Moreover, anti-MHC class I monoclonal antibodies also stimulated intercellular adherence. Adhesion induced upon MHC engagement was faster and stronger than that triggered by phorbol esters. It needed active metabolism, but divalent cations were not required. Monoclonal antibodies directed against LFA-1 (CD11a/CD18) or its ligand ICAM-1 (CD54) did not inhibit MHC class II-induced homotypic adhesion of various EBV-transformed B cell lines, nor of a variant of the B cell line Raji expressing very low LFA-1 surface levels. Moreover, EBV-transformed B cells from a severe lymphocyte adhesion deficiency patient, lacking surface CD11/CD18, also aggregated in response to anti-MHC class I or class II monoclonal antibodies. Together these data indicate that engagement of MHC molecules may transduce signals to B cells resulting in up-regulation of intercellular adhesion, via an LFA-1-independent mechanism. This may play a role in the stabilization of T cell/antigen-presenting cell conjugates at the moment of antigen recognition.
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PMID:Engagement of major histocompatibility complex class I and class II molecules up-regulates intercellular adhesion of human B cells via a CD11/CD18-independent mechanism. 134 12

Otitis media develops when certain bacterial pathogens gain access to the middle ear cavity from the nasopharynx through the eustachian tube. Adhesion of bacteria, in particular Streptococcus pneumoniae and Haemophilus influenzae, to the non-ciliated epithelial cells of the nasopharynx, close to the opening of the eustachian tube, is significantly correlated to the otitis-prone condition in children. Otitis-prone children have significantly fewer bacteria in the nasopharynx coated with the immunoglobulin secretory IgA (SigA) then healthy children have. Adhesion and occurrence of middle ear pathogens in the nasopharynx decreases with advancing age. Epstein-Barr virus, causative agent of infectious mononucleosis, causes a remarkable increase in bacterial adhesion to epithelial cells.
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PMID:[Bacterial adhesion to epithelial cells of the nasopharynx essential in the development of otitis media]. 144 42

The occurrence of recurrent bacterial infections, neutrophil motility dysfunction and normal expression of beta 2 integrins (CD18) in two unrelated children suggested an as yet undescribed adhesion deficiency. The fact that both children exhibited the rare Bombay blood group and were Lewis negative, each involving carbohydrates with different fucose linkages, suggested a possible defect in the fucose-containing ligand for E- and P-selectin, sialyl Lewis X (SLe(x)). Using a monoclonal anti-SLe(x) antibody, we did not detect expression of SLe(x) on the neutrophils of the patients. Adhesion of neutrophils to endothelial cells activated with interleukin-1 beta or histamine was markedly decreased ( < 5% of control). The observation that the neutrophils did not bind to recombinant E-selectin and purified P-selectin confirmed the SLe(x) deficiency as the basis for adhesion deficiency. Using several in vivo techniques, we were able to show that neutrophil rolling, the first step in their adhesion, is markedly decreased, and therefore neutrophil emigration through the endothelium and arrival at site of inflammation is significantly diminished (1-2% of normal). Low binding of fucose-specific lectins to the patients' B lymphocytes transformed with Epstein-Barr virus was observed, while the binding of mannose-specific lectins was normal, providing further evidence for a general fucose deficiency as the primary defect. The existence of the patients and their deficiency emphasizes the essential role of the endothelial cell selectins and their ligand, SLe(x), in recruitment of neutrophils to sites of infection.
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PMID:Leukocyte adhesion deficiency (LAD) II. 758 37

We analyzed the cell-cell adherence related to CD11/CD18 and CD18 mRNA in individuals with decreased CD11/CD18 expression on their neutrophil surface. Epstein Barr virus-transformed B cell lines were developed from one localized juvenile periodontitis (LJP) patient with decreased CD11/CD18 in the peripheral blood neutrophils and without systemic diseases; two siblings with generalized prepubertal periodontitis (GPP) caused by leukocyte adhesion deficiency (LAD); another LJP patient; one localized prepubertal periodontitis (LPP) patient; and two healthy subjects. Adhesion of leukocytes to each other was measured as cluster formation by aggregation assay. The length and the amount of CD18 mRNA expressed in the cell lines were analyzed by Northern blotting using the 32P-labeled CD18 cDNA. The coding region of the mRNA was analyzed by the reverse transcription-polymerase chain reaction method. Base-mismatches between CD18 mRNA and the 32P-labeled RNA probe synthesized from CD18 cDNA were analyzed by RNase protection assay. In the adherence assay, cells from the LJP patients with decreased CD11/CD18 formed more clusters of smaller size and fewer cells than those of the other subjects. The cells from GPP and LAD patients did not aggregate and did not form clusters either in the absence or presence of PMA. There were no differences in the length and the amount of mRNA between the LJP patients and the other subjects, while GPP-LAD patients expressed a small amount of long mRNA. The whole coding region (2,313 base pairs) of all subjects was amplified except for the GPP-LAD patients, and the 5'-region (1,119 base pairs) was amplified from all subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular basis of leukocyte adhesion molecules in early-onset periodontitis patients with decreased CD11/CD18 expression on leukocytes. 782 77

We investigated 49 acquired immunodeficiency syndrome-related lymphomas (ARLs) for Epstein-Barr virus (EBV) by Southern blotting and in situ hybridization and, in positive cases, used cryostat immunohistology to compare EBV-latent gene expression (EBV encoded small RNA-1 [EBER-1], EBV nuclear antigen-2 [EBNA-2], latent membrane protein-1 [LMP-1] and host cell immunophenotype (CD11a, CD18, CD54, CD58, CD21, CD23, CD30, CD39, CDw70, immunoglobulin) patterns with those reported in other EBV infections. EBV+ immunoblast-rich/large cell ARLs (n = 22) showed three patterns of latency: broad (EBER+EBNA-2+/LMP-1+; n = 9), reminiscent of a lymphoblastoid cell line phenotype; restricted (EBER+/EBNA-2-/LMP-1-; n = 6), similar to endemic Burkitt's lymphoma; and intermediate (EBER+/EBNA-2-/LMP-1+; n = 7), a pattern rarely described in vitro but seen in certain EBV-related malignancies. EBNA-2 expression was associated with extranodal lymphomas. EBV+ Burkitt-type ARLs (n = 11) usually showed the restricted latency pattern (n = 8), but some expressed the intermediate form (n = 3). Adhesion (CD54, CD58) and activation (CD30, CD39, CDw70) molecule expression varied with morphology (immunoblast-rich/large cell versus Burkitt-type), but was not independently correlated with EBV-positivity. CD30 and LMP-1 expression were associated. ARLs show heterogeneity regarding both the presence of EBV and latency pattern. Comparison of these phenotypically distinct lymphoma groups with known forms of EBV infection provides clues to their possible pathogenesis.
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PMID:Epstein-Barr virus-latent gene expression and tumor cell phenotype in acquired immunodeficiency syndrome-related non-Hodgkin's lymphoma. Correlation of lymphoma phenotype with three distinct patterns of viral latency. 821 3

We report a non-HIV patient who had B chronic lymphocytic leukemia (CLL) with progressive multifocal leukoencephalopathy (PML) and diffuse cerebral leukemic parenchymal infiltration in the presence of JC virus and Epstein-Barr virus (EBV) cerebral co-infection. Multiple subcortical hypodensities lining the cortico-subcortical junction were present within the white matter on computerized tomography (CT) scan, with large areas of high signal intensity on T2-weighted sequences on magnetic resonance imaging (MRI). JCV DNA was identified in peripheral blood nuclear cells and cerebrospinal fluid polymerase chain reaction (PCR) DNA/DNA hybridization plus Southern blot analysis. Frontal stereotactic biopsy confirmed the diagnosis of PML by immunocytochemistry, in situ hybridization (ISH) with JC Enzo probe and electron microscopy. Leukemic B cells with the same phenotype as leukemic blood cells were disseminated in the demyelinated areas. They were labeled by anti-latent membrane protein and by BamHl W EBV probe after ISH. Adhesion and activation molecules were positive for CD23. Autopsy showed diffuse visceral leukemic infiltration without acutization. EBV-transformed B lymphocytes would favour JCV penetration and/or intracerebral reactivation of previously latent JCV infection with further development of simultaneous PML and cerebral CLL infiltration in an immunosuppressed patient.
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PMID:Simultaneous progressive multifocal leukoencephalopathy, Epstein-Barr virus (EBV) latent infection and cerebral parenchymal infiltration during chronic lymphocytic leukemia. 830 57

Adhesion to cells and matrices participates in the regulation of lymphocyte proliferation, maturation and tissue localization. Consequently, abnormal patterns of adhesion molecule expression may contribute to the pathophysiology of lymphoproliferative disorders. Integrins are major cell-surface adhesive proteins composed by alpha and beta subunits. In contrast to normal lymphocytes, Burkitt's lymphoma (BL) cells lack the beta2 integrin CD11a/CD18. To study the molecular mechanism underlying this deficiency, presence of the transcript for each subunit was analysed by Northern blotting in group I BL lines (BL biopsy-like) and, for comparison, Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs). While transcripts for both CD11a (alpha subunit) and CD18 (beta subunit) were readily detected in LCLs, BL lines contained the transcript for the alpha subunit only. Treatment of BL cells with phorbol ester for 72 h induced expression of the beta subunit mRNA and the CD11a and CD18 antigens on the cell surface. The results indicate that the CD11a/CD18 deficiency of BL is due to absence of the beta subunit transcript and that this defect is restored by stimulation of the cells.
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PMID:Adhesion molecule CD11a/CD18-deficient Burkitt's lymphoma cells lack the transcript for the beta, but not the alpha, integrin subunit. 902 Mar 71

Hepatocyte growth factor (HGF)/scatter factor (SF) is the ligand for a tyrosine kinase cell surface receptor encoded by the MET protooncogene (c-MET). HGF/SF can induce proliferation and motility in epithelial cells and promotes invasion of carcinoma cells and NIH3T3 fibroblasts transfected with both HGF/SF and c-MET genes. Our results show that HGF/ SF and c-MET also play a role in adhesion and invasion of human lymphoma cells. c-MET mRNA is expressed in hemopoietic cells, such as hemopoietic progenitor cells (CD34+ cells) in bone marrow (BM) and mobilized peripheral blood, immature B cells in cord blood and BM, and germinal center B-centroblasts. In normal peripheral blood B cells, which are c-MET-, c-MET expression was induced by PMA, ConA, HGF/ SF, and Epstein-Barr virus (EBV) infection. Using immunohistochemistry, we detected c-MET on the cell surface of large activated centroblasts in lymph nodes from patients with B-non-Hodgkin's lymphoma and Hodgkin's disease. In the latter group, c-MET expression correlated well with the presence of EBV. Because HGF/SF and c-MET promote metastasis of carcinoma cells, we studied the effects of c-MET stimulation by HGF/SF of B-lymphoma cells on properties relevant for metastasis, ie, adhesion, migration, and invasion. HGF/SF stimulated adhesion of the c-MET+ B-cell lines to the extracellular matrix molecules fibronectin (FN) and collagen (CN) in a dose dependent manner. However, adhesion to laminin was not affected by HGF/SF. Adhesion to FN was mediated by beta 1-integrins alpha 4 beta 1 (VLA4) and alpha 5 beta 1 (VLA5) since blocking antibodies against beta 1- (CD29), alpha 4-(CD49d), or alpha 5- (CD49e) integrin subunits, completely reversed the effect of HGF/SF. Furthermore, HGF/SF induced adhesion was abrogated by addition of genistein, which blocks protein tyrosine kinases, including c-MET. Addition of HGF/SF resulted in a sixfold increase in migration of c-MET B-lymphoma cells through Matrigel, compared to medium alone. In rat fibroblast cultures, HGF/SF doubled the number of c-MET+ B-lymphoma cells that invaded the fibroblast monolayer. In these adhesion, migration and invasion assays HGF/SF had no effect on c-MET- cell lines. In conclusion, c-MET is expressed or can be induced on immature, activated, and certain malignant B cells. HGF/SF increased adhesion of c-MET+ B-lymphoma cells to FN and CN, mediated via beta 1-integrins alpha 4 beta 1 and alpha 5 beta 1, and furthermore promoted migration and invasion.
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PMID:Hepatocyte growth factor/scatter factor promotes adhesion of lymphoma cells to extracellular matrix molecules via alpha 4 beta 1 and alpha 5 beta 1 integrins. 902 31

Members of the interleukin (IL)-12 family constitute subunits of IL-12, -23, and -27. These ILs represent pivotal mediators in the regulation of cell-mediated immune responses and in animal models of human inflammatory bowel disease. Recent work has suggested that intestinal endothelial cells might serve as a second line of defense in bacterial sensing of invading pathogens. The purpose of this study was to examine the production of IL-12 family members in intestinal endothelial cells (HIMEC). HIMEC were stimulated with proinflammatory agents (TNF-alpha, IFN-gamma, IL-1beta) and microbial antigens [LPS, lipoteichoic acid, peptidoglycan, CpG-DNA, flagellin, poly(I:C)]. Expression of IL-12 family members and of Toll-like receptor (TLR)3 in HIMEC was assessed by real-time RT-PCR, immunostaining, flow cytometry, and immunoblot analysis. HIMEC display an induction of Epstein-Barr virus-induced gene 3 (EBI3), IL-12p35, and IL-23p19, whereas no expression of IL-12p40 and IL-27p28 was detectable. The strongest induction was induced by proinflammatory factors known to utilize the NF-kappaB pathway, and expression of EBI3 and IL-23p19 was diminished by an NF-kappaB inhibitor. HIMEC display regulated expression of TLR3. Adhesion and transmigration assays showed proinflammatory responses after HIMEC stimulation. HIMEC are capable of producing IL-12 family members as a response to microbial stimuli. The TLR3 agonist, poly(I:C), was shown to enhance leukocyte adhesion in vitro in HIMEC. Our data suggest that the intestinal microvasculature is responsive to ligands of TLR3 expressed on intestinal endothelial cells, thereby adding to the regulation of adaptive immunity and leukocyte recruitment.
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PMID:Expression of IL-12-related molecules in human intestinal microvascular endothelial cells is regulated by TLR3. 1794 55