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)

Intercellular adhesion molecule-1 (ICAM-1) expression by tumour cells may be involved in their interaction with defensive cells. In this study the surface ICAM-1 expression and soluble ICAM-1 (sICAM-1) production by five small cell lung cancer (SCLC) and five non-SCLC (NSCLC) cell lines was investigated. In addition, the effects of ICAM-1 upregulation by cytokines on the adhesion of lung cancer cells to allogeneic lymphokine-activated killer (LAK) cells and susceptibility to LAK cytotoxicity was also evaluated. ICAM-1 expression was assessed by flow cytometry. Soluble ICAM-1 release was measured by enzyme-linked immunosorbent assay (ELISA). Interaction with LAK cells was tested by adhesion and cytotoxicity assays. At baseline, SCLC lines did not express ICAM-1, while 4 of the 5 NSCLC lines expressed ICAM-1. ICAM-1 expression was induced by interferon-gamma (IFN-gamma) in 4 of the 5 SCLC lines and upregulated in 1 of the 5 NSCLC lines. ICAM-1 expression was induced by tumour necrosis factor-alpha (TNF-alpha) in 1 of the 5 SCLC lines (National Cancer Institute (NCI) H211), and upregulated in 2 of the 5 NSCLC lines (NCI H460 and NCI H838). Among the latter lines, one (NCI H838) released significant amounts of sICAM-1. Adhesion to LAK cells and susceptibility to LAK cytotoxicity were significantly higher in TNF-alpha-treated NCI H460 and NCI H211 cells, compared to untreated NCI H460 and NCI H211 cells. In contrast, no difference in adhesion to LAK cells and susceptibility to LAK cytotoxicity was detected between baseline and TNF-alpha-treated NCI H838 cells. Intercellular adhesion molecule-1 surface expression and soluble intercellular adhesion molecule-1 release may play an important role in interactions between lymphokine-activated killer cells and lung cancer cells.
 ...
PMID:ICAM-1 expression by lung cancer cell lines: effects of upregulation by cytokines on the interaction with LAK cells. 888 99

Nine cases of rheumatic fever were seen from 1982 to 1996. The diagnosis was based on Jones criteria. Four of eight children had carditis characterized by mitral regurgitation with or without aortic regurgitation and/or atrioventricular conduction disturbances. The outcome was favorable in all the patients who had carditis initially; one of the patients without initial carditis developed permanent cardiac lesions during a recurrence with carditis. In industrialized countries, the incidence of rheumatic fever declined starting early in the XXth century, then dropped sharply after World War II, and is now extraordinarily low (mean annual incidence, 0.5/100,000 schoolage children). In developing countries, by contrast, rheumatic fever was recognized only after World War II and remains endemic (mean annual incidence, 100 to 200/100,000 schoolage children), contributing a substantial proportion of cases of cardiovascular disease. The diagnosis is difficult and rests on clinical grounds since there is no specific laboratory test. Diagnostic delays are potentially serious. Acute attacks should be managed as therapeutic emergencies. Prevention of recurrences rests on long-term antimicrobial therapy. Rheumatic fever is a disease process resulting from an inappropriate immune response to pharyngitis due to a beta-hemolytic group A streptotoccus (BHAS). A low standard of living may be a factor in developing countries but fails to explain the epidemic flares seen in these areas or the residual background incidence in industrialized countries. A role of host-related susceptibility to the disease has not been demonstrated. The type-specific surface M protein, the main factor associated with high virulence, carries a specific epitope on its distal portion. Rheumatogenic strains have been identified; most produce mucoid colonies. At a given point in time, within a given serotype, the virulence of a specific strain increases. Temporal and spatial variations of observed types contribute additional complexity. Adhesion of the organisms is followed by release of streptococcal degradation products that share antigenic determinants with human tissues including the heart, the synovium, and the neurons. The hyaluronate capsule and M protein of the organisms are capable of initiating immune responses; their presentation to CD4+ T-cells results in lymphokine production, an acute phase humoral response, and a cell-mediated response potentially responsible for permanent valvular damage. In France, the standard of care is to prescribe antimicrobial therapy to all patients with pharyngitis or tonsillitis without performing tests to identify the causative agent. The introduction of tests for the rapid recognition in routine clinical practice of BHAS, which account for only 20 to 30% of all cases of pharyngitis and tonsillitis, should allow a more rational approach to the treatment of these infections. Reserving antimicrobial therapy to those patients with BHAS should not result in an increase in the incidence or rheumatic fever.
 ...
PMID:[Acute articular rheumatism in the child in 1997]. 992 98

The intercellular adhesion molecule-1 (ICAM-1, CD54) serves as a counter-receptor for the beta2-integrins, LFA-1 and Mac-1, which are expressed on leukocytes. Although expression of ICAM-1 on tumor cells has a role in tumor progression and development, information on ICAM-1 expression and its role in oral cancer has not been established. Normal human oral keratinocytes (NHOK), human papilloma virus (HPV)-immortalized human oral keratinocyte lines (HOK-16B, HOK-18A, and HOK-18C), and six human oral neoplastic cell lines (HOK-16B-BaP-T1, SCC-4, SCC-9, HEp-2, Tu-177 and 1483) were used to study ICAM-1 expression and its functional role in vitro. Our results demonstrated that NHOK express negligible levels of ICAM-1, whereas immortalized human oral keratinocytes and cancer cells express significantly higher levels of ICAM-1, except for HOK-16B-BaP-T1 and HEp-2. Altered mRNA half-lives did not fully account for the increased accumulation of ICAM-1 mRNA. Adhesion of peripheral blood mononuclear cells (PBMC) to epithelial cells correlated with cell surface ICAM-1 expression levels. This adhesion was inhibited by antibodies specific for either ICAM-1 or LFA-1/Mac-1, suggesting a role for these molecules in adhesion. In contrast, lymphokine-activated-killer (LAK) cell cytotoxic killing of epithelial cells did not correlate with ICAM-1 levels or with adhesion. Nonetheless, within each cell line, blocking of ICAM-1 or LFA-1/Mac-1 reduced LAK cell killing, suggesting that ICAM-1 is involved in mediating this killing.
 ...
PMID:Increased ICAM-1 expression in transformed human oral epithelial cells: molecular mechanism and functional role in peripheral blood mononuclear cell adhesion and lymphokine-activated-killer cell cytotoxicity. 1093 87

NK cells are key mediators of the innate immune response and anti-tumor surveillance. Adhesion and degranulation-promoting adapter protein (ADAP, formerly known as SLAP-130 or Fyb) is a hematopoietic-specific adapter that is required for efficient TCR signaling and T cell activation. Herein, we examine a potential role for ADAP in NK development and function. ADAP is expressed in primary NK cells and in IL-2 stimulated lymphokine-activated killers. However, ADAP-deficient mice show no defects in NK development. Further, ADAP is dispensable for key NK functions, including cytotoxicity in response to engagement of activating receptors, cytokine production, conjugate formation and tumor suppression in vivo. These results indicate that, unlike events stimulated by TCR engagement, signaling events engaged by immunoreceptor tyrosine-based activation motif-associated and cytokine receptors on NK cells can occur independently of ADAP.
 ...
PMID:ADAP is dispensable for NK cell development and function. 1677 24