Viewing affirmative mentions of gene expression of ICAM1 (H. sapiens) in T cells

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Motoya et al. (1997)intercellular adhesion molecule-1T-cellAssociation between expression of intercellular adhesion molecule-1 and integration of human T-cell-leukemia virus type 1 in adult T-cell leukemia cells.
Motoya et al. (1997)intercellular adhesion molecule-1T cellIt is known that the expression levels of intercellular adhesion molecule-1 (ICAM-1) in adult T cell leukemia(ATL) cells are high, whereas those in T-lymphoid cells are not.
Lewis et al. (1989)ICAM-1T cellsICAM-1 expression by epidermal cells appears to be closely linked to the progressive migration of T cells from the dermis into the epidermis that characterizes cutaneous delayed hypersensitivity.
Tsukada et al. (1994)ICAM-1T cellsTo investigate the origin of intercellular adhesion molecule-1 (ICAM-1) and its expression on brain endothelial cells, we studied the expression in vitro of ICAM-1 on human brain endothelial cells after incubation of T cells from patients with multiple sclerosis (MS) using a histochemical technique and flow cytometry.
De Luca et al. (1997)ICAM-1T cellsWe have previously demonstrated that in vitro exposure of antigen-presenting cells to UVB radiation inhibits their ability to activate T cells through selective effects on the expression of the adhesion molecule ICAM-1 (intercellular adhesion molecule-1).
Nakayama et al. (1996)ICAM-1T-cellsA significant relationship was seen between the incidence of ICAM-1 expression on T-cells and the number of days from the initiation of radiotherapy to the onset of radiation pneumonitis.
Viac et al. (1992)ICAM1T cellsEpidermotropism of T cells correlates with intercellular adhesion molecule (ICAM1) expression in human papillomavirus (HPV)-induced lesions.
Hu et al. (2010)ICAM-1T cellsIn addition, miR-221-mediated expression of ICAM-1 on cholangiocytes showed a significant influence on the adherence of cocultured T cells.
Piela-Smith and Liu (2001)ICAM-1T-cellThe decrease in ICAM-1 expression was accompanied by a decrease in T-cell adhesion to the treated fibroblasts.
Tohma et al. (1992)ICAM-1T cellsResting CD4+ T cells were largely ICAM-1 negative, whereas immobilized anti-CD3 monoclonal antibody (mAb) rapidly induced ICAM-1 expression.
Tohma et al. (1992)ICAM-1T cellThese findings suggest that rapid changes in density of ICAM-1 expression and the mobility of ICAM-1 on activated T cells may play a role in providing activation signals to B cells during T cell-B cell collaboration.
Buckle and Hogg (1990)ICAM-1T cellWe have shown that low levels of intercellular adhesion molecule-1 (ICAM-1) expression can be detected on approximately 40% of the resting peripheral blood T cell population.
Buckle and Hogg (1990)ICAM-1T cellsIn addition we have shown that the cytokines interleukin 2 and interferon-gamma, both of which are products of activated T cells, are able to increase the expression of ICAM-1 on T cells.
Roy et al. (2001)ICAM-1T cellsIntercellular adhesion molecule-1 (ICAM-1) gene expression in human T cells is regulated by phosphotyrosyl phosphatase activity.
Roy et al. (2001)ICAM-1 geneT cellsThe use of bis-peroxovanadium (bpV) compounds, a class of potent PTP inhibitors, enabled us to investigate the involvement of phosphotyrosyl phosphatases in the regulation of ICAM-1 gene expression in human T cells.
Roy et al. (2001)ICAM-1T cellsAltogether, these observations suggest that expression of ICAM-1 in human T cells is regulated by phosphotyrosyl phosphatase activity through NF-kappaB-, Ets-, and STAT-1-dependent signaling pathways.
Schierloh et al. (2009)ICAM-1T-cellWe found that endogenously activated pleural fluid-derived NK cells express high ICAM-1 levels and induce T-cell activation ex vivo through ICAM-1.
Imai et al. (1993)CD54T-cellPreviously, we studied the surface expression of LFA-1 (CD11a/CD18) and ICAM-1 (CD54) in a panel of 16 human T-cell lines and found that those carrying HTLV-1 pro-viruses expressed high levels of ICAM-1.
Boussiotis et al. (1993)ICAM-1T lymphocytesHere, we show that transfectants expressing HLA-DR7 and either B7 or intercellular adhesion molecule 1 (ICAM-1) deliver independent costimulatory signals resulting in alloantigen-induced proliferation of CD4-positive T lymphocytes.
Boyd et al. (1989)ICAM-1T cellsWhen B cells, T cells, macrophages, or granulocytes were activated in vitro by suitable mitogens, ICAM-1 expression was induced in all cases.
Kato et al. (2003)ICAM-1T cellHowever, another ICAM-1(low) human cell line as well as murine tumor cell lines pulsed with pamidronate remained totally defective in gammadelta T cell activation even after expression of human ICAM-1.
Hviid et al. (1993)ICAM-1T-cellKinetics of human T-cell expression of LFA-1, IL-2 receptor, and ICAM-1 following antigenic stimulation in vitro.
Hviid et al. (1993)ICAM-1T-cellWhile this is in agreement with previous reports of the expression kinetics of IL-2R and ICAM-1, this is the first report indicating that the regulation of T-cell surface expression of LFA-1 is bidirectional.
Piela-Smith et al. (1991)ICAM-1T lymphocytesWe have compared the ability of ICAM-1 expressed on the surface of human fibroblasts (FB) to function as a receptor for HRV as well as a receptor for LFA-1-bearing human T lymphocytes.
Andersen (1997)ICAM-1T-lymphocytesImmunohistochemically, strong expression of ICAM-1, vascular cellular adhesion molecule-1 and MHC class II antigens on tubular and endothelial cells along with interleukin-2-receptor bearing infiltrates of T-lymphocytes and significant presence of macrophages were highly correlated with acute rejection.
Nickoloff et al. (1992)intercellular adhesion molecule-1T cellsA growing body of data strongly supports the in vivo role of lymphocyte-function-associated antigen-1 (CD18) expression by T cells in the binding to intercellular adhesion molecule-1 (CD54) expressing keratinocytes.
Altmann et al. (1989)ICAM-1T-cellWe have investigated the role of LFA-1/ICAM-1 interactions in antigen presentation directly by quantifying the contribution of ICAM-1 expression to T-cell stimulation using L-cell transfectants that co-express ICAM-1 and HLA-DR.
Altmann et al. (1989)ICAM-1T-cellIn the case of transfectants expressing modest levels of HLA-DR, co-expression of ICAM-1 is critical for effective HLA class II-restricted and allospecific T-cell activation, pointing to an important role for ICAM-1 in the induction of T-cell responses.
Waldorf et al. (1991)ICAM-1T-cellIntrafollicular T-cell migration occurred independent of ICAM-1 expression and commenced as early as 4 hours after challenge.
Viita et al. (1999)intercellular adhesion molecule 1T-cellThese cells were used to study the effects of 15-LO on the expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1), activation of nuclear factor kappa B (NF-kappaB), and T-cell adhesion on endothelial cells.
Lazaar et al. (1997)ICAM-1T cellsAntigen receptor-stimulated peripheral blood and bronchoalveolar lavage-derived T cells induce MHC class II and ICAM-1 expression on human airway smooth muscle.
Lazaar et al. (1997)ICAM-1T cellsFurthermore, in studies with bronchoalveolar lavage-derived T cells isolated from atopic donors following local antigen challenge, we observed adhesion to ASM and upregulation of ASM expression of ICAM-1 and HLA-DR similar to that seen with in vitro-activated T cells.
Lazaar et al. (1997)ICAM-1T cellsFinally, we found that despite expression of ICAM-1 and HLA-DR, ASM could not present alloantigen to CD4+ T cells.
Kim et al. (2000)ICAM-1T-lymphocytesThese study results suggest that HSV induces the increased expression of ICAM-1, or induction of VCAM-1 and E-selectin on HDMEC and that among these adhesion molecules, the expression of ICAM-1 on HDMEC mainly regulates the binding of T-lymphocytes to HDMEC.
Piela-Smith et al. (1992)ICAM-1T lymphocyteThe kinetics of increased ICAM-1 expression induced by IL-4 paralleled the increase in ICAM-1-dependent T lymphocyte adhesion.
Jin et al. (1994)ICAM-1T-cellCutaneous lesions of T-cell proliferative disorders are characterized by epidermotropic infiltration of the neoplastic cells and expression of intercellular adhesion molecule-1 (ICAM-1) and HLA-DR by lesional keratinocytes.
Fukudome et al. (1992)ICAM-1T-cellSixteen human T-cell lines were studied for the expression of a cell-adhesion molecule ICAM-1 and its counter-receptor LFA-1.
Calhoun et al. (1999)ICAM-1T cellsInhibition was not associated with altered cell surface expression of receptors such as CD3, CD4, ICAM-1, LFA-1, CD25, and HLA-DR however, these antibodies did impede the ability of generation of functionally active T cells.
Chan et al. (1999)ICAM-1T-cellsIn addition, these T-cells did not express IL2-receptors and expression of CD54 (ICAM-1) and CD58 (LFA-3) resembled that of resting T-cells.
Lee et al. (1999)ICAM-1T lymphocytesThese results show that AECA-positive sera of Behçet's disease patients are capable of activating HDMEC to promote the adherence of T lymphocytes to increase the expression of ICAM-1, VCAM-1, and E-selectin on the cell surfaces.
Tanaka et al. (1996)intercellular adhesion molecule 1T-cellPreviously, we showed that surface expression of intercellular adhesion molecule 1 (ICAM-1) was strongly upregulated in T cells carrying proviral human T-cell leukemia virus type 1 (HTLV-1) and that the viral transactivator protein Tax1 was capable of inducing the ICAM-1 gene.
Seko et al. (1995)ICAM-1T-cellsPerforin may have directly injured myocardial cells which showed marked expression of human leukocyte antigens (HLAs) and intercellular adhesion molecule-1 (ICAM-1) as well as costimulatory molecules B7 and B70, which are ligands for CD28 expressed on T-cells.
Murphy et al. (1993)intercellular adhesion molecule-1T-cellEnhanced expression of intercellular adhesion molecule-1 (ICAM-1) and human leukocyte antigen (HLA)-DR by melanoma cells were invariably associated with zones of T-cell infiltration, whereas diminished or absent expression was observed in relatively unaffected regions of tumors.
Ishikura et al. (1991)ICAMT cellsThese data suggest that cytokines, especially IFN-gamma, TNF-alpha, and IL-1 alpha/beta, released by T cells and antigen-presenting cells upon recognition of alloantigens upregulate ICAM-1 expression on renal tubular epithelial cells.
Owen et al. (1997)ICAMT cellsIn vitro infection of T cells with human T lymphotropic virus types I and II (HTLV-I and HTLV-II) resulted in constitutive expression of ICAM-1.
O'Brien et al. (1996)ICAM-1T-lymphocyteIncreased plaque intimal T-lymphocyte density was associated with the presence of both ICAM-1 and VCAM-1 on neovasculature (both P < .01) and on nonendothelial cells (both P < .01).
Costello et al. (1998)CD54T lymphocytesAML cell stimulation via CD40: (1) significantly improved IL-2 secretion but not proliferation of responding T lymphocytes, (2) increased CD54/ICAM-1 expression in three quarters of cases, (3) failed in most cases to induce CD40-specific CD80/B7-1 up-regulation, and (4) had a weak effect on CD86/B7-2 expression.
Stachowski et al. (1994)ICAM-1T cellsWe have found that the cause of the blunted response to HBV vaccination is multifactorial and seems to be associated with the following: (1) A reduced number of TCR/CD3 antigen receptor complexes on freshly isolated uraemic CD4 T cells, especially in non-responders. (2) The blunted proliferative response of uraemic CD4 T cells isolated from non-responders and stimulated for 6 days by autologous monocytes presenting HBsAg was associated with the decreased density of the TCR/CD3 receptors. (3) Moreover, in uraemic non-responders the expression of adhesion and accessory molecules on monocytes (intercellular adhesion molecule-1/ICAM-1, HLA-DR/Ia/) was significantly decreased following the culture with autologous monocytes serving as HBsAg-presenting cells.
Boorstein et al. (1994)ICAM-1T-lymphocyteAberrant cellular expression of HLA-DR and intercellular adhesion molecule-1 (ICAM-1), both of which are necessary for optimal antigen-induced T-lymphocyte responses, is present in lesions of HSK, but little is known concerning endogenous cytokines that may inhibit HLA-DR or ICAM-I expression in human disease.
Wake et al. (1995)ICAM-1T cellsWe report the following novel features of homotypic adhesion via leukocyte function-associated antigen-1 (LFA-1)/intracellular adhesion molecule-1 (ICAM-1) pathway that suggest a role for it in cytokine production and rapid proliferation of ATL cells: (1) ATL cells show clustering in a calcium dependent manner, even at the higher concentration; (2) ATL cells consistently and highly express ICAM-1 and an active form of LFA-1, whereas integrin expression, except for LFA-1, is rather lower compared with that of normal CD4+ T cells; (3) ATL cells make conjugate formation within 6 minutes and clustering within 48 hours, both of which are inhibited by the addition of monoclonal antibodies (MoAbs) against LFA-1 and ICAM-1; (4) spontaneous mRNA transcription and protein secretion of both interleukin-1 and parathyroid hormone-related protein are observed consistently in ATL cells, and these productions are inhibited by anti-LFA-1 and anti-ICAM-1 MoAbs but are markedly increased by cross-linking of LFA-1 and ICAM-1 by the immobilized specific MoAbs; and (5) proliferative responses of ATL cells are also inhibited by these MoAbs.
Farmer et al. (2001)CD54T-cellFurthermore, when the SVpgC2a cell line was treated with T-cell derived cytokines, upregulation of CD40 expression was observed when the cells were treated with IL-4, whereas IFN-gamma caused upregulation in expression of CD40, CD54 and MHC class II.
Liu et al. (2009)ICAMT cellsCONCLUSION: In vitro, the expression of ICAM-1 or ICAM-2 on human pancreatic cancer cells is critically important in determining the extent to which these cells are sensitive to killing by human gammadelta-T cells.
Liu et al. (2009)ICAMT cellsExpression of intercellular adhesion molecule (ICAM)-1 or ICAM-2 is critical in determining sensitivity of pancreatic cancer cells to cytolysis by human gammadelta-T cells: implications in the design of gammadelta-T-cell-based immunotherapies for pancreatic cancer.
Liu et al. (2009)ICAMT cellsAccordingly, in ongoing and future clinical studies using gammadelta-T cells for the treatment of a variety of epithelial-derived solid tumors-including pancreatic cancer-interventions intended to modulate ICAM expression on tumor cells may become important adjuncts to gammadelta-T-cell-based immunotherapies.
Briscoe et al. (1995)intercellular adhesion molecule-1T cellThe expression of endothelial adhesion molecules intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin, as well as the presence of CD3+ T cell infiltrates was assessed by immunocytochemical staining of frozen sections.
Geiselhart et al. (1997)ICAM-1T-lymphocyteThe cigarette tar component p-benzoquinone blocks T-lymphocyte activation by inhibiting interleukin-2 production, but not CD25, ICAM-1, or LFA-1 expression.
Wittig et al. (1997)ICAM-1T-cellsA cell adhesion assay revealed that the enhanced adhesion on T-cells to tumor cells mediated by soluble E-selectin-induced ICAM-1 expression was at a maximum after a 12-h incubation period.
Tanaka et al. (1995)ICAM-IT-cellInduction of TaxI in a human T-cell line Jurkat carrying the TaxI gene under the metallothionein promoter led to increases in mRNA and surface expression of ICAM-I.
Lenz et al. (1993)ICAM-1T cellsThe dermal cells have the following key features of mature DC: (a) sheet-like processes, or veils, that are constantly moving; (b) very high levels of surface MHC products; (c) absence of markers for macrophages, lymphocytes, and endothelium; (d) substantial expression of adhesion/costimulatory molecules such as CD11/CD18, CD54 (ICAM-1), B7/BB1, CD40; and (e) powerful stimulatory function for resting T cells.
Kanno et al. (2008)intercellular adhesion molecule-1T cellSNKs expressed intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) at much higher levels than those in EBV-negative T cell lines.
Kanno et al. (2008)ICAM-1T cellSNKs produced the larger amount of tumour necrosis factor (TNF)-alpha, which caused increased expression of ICAM-1 and VCAM-1 in cultured human endothelial cells, than that from EBV-negative T cell lines.
Porter and Hall (2009)ICAM-1T cellsIn conclusion, we show that egression of T cells involves three distinct sequential steps: adhesion, junctional recognition, and diapedesis; we further demonstrate that ICAM-2 is expressed on the bronchial epithelium and, together with ICAM-1, has an essential function in the clearance of T cells from the lung.
Banks et al. (2000)CD54T lymphocytesNo major changes in T cell subsets were seen but expression of CD25 and CD54 by T lymphocytes significantly increased, accompanied by marked increases in soluble CD25 (sIL-2R) and CD54 (sICAM-1).
Makino et al. (1999)CD54T cellsAutoreactive T cells from patients with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) spontaneously proliferate in vitro, and their activation is reported to be associated with CD54 expression.
Hakonarson et al. (2001)CD54T cellsExtended studies demonstrated that: 1) ASM cells express mRNAs and proteins for the cell adhesion molecules (CAMs)/costimulatory molecules, CD40, CD40L, CD80, CD86, ICAM-1 (CD54), and LFA-1 (CD11a/CD18); 2) apart from LFA-1, ASM cell surface expression of the latter molecules is up-regulated in the presence of activated T cells; and 3) pretreatment of ASM cells and tissues with mAbs directed either against CD11a or the combination of CD40 and CD86 completely abrogated both the activated T cell-induced changes in expression of the above CAMs/costimulatory molecules in ASM cells and altered ASM tissue responsiveness.
Bonham et al. (2003)intracellular adhesion molecule-1T cellsAlterations in circulating levels of B cells (cluster of differentiation (CD) 19), memory T cells (CD45RO) and expression of the intracellular adhesion molecule-1 (CD54) on T cells were observed.
Batten et al. (1995)intercellular adhesion molecule-1T cellsDAP.3 transfectants expressing native H-2E molecules with or without human LFA-3 and ICAM-1 (intercellular adhesion molecule-1) failed to induce proliferation by human peripheral blood T cells.
Tandon et al. (1992)intercellular adhesion molecule-1T cellThyroid follicular cells from patients with Graves' disease and Hashimoto's thyroiditis express intercellular adhesion molecule-1 (ICAM-1) and this is in part responsible for T cell adherence in vitro.
Tandon et al. (1992)ICAM-1T cellsThese results show that two important adhesion receptor ligands, ICAM-1 and LFA-3, are expressed by thyroid cells in autoimmune thyroiditis and that these are likely to have functional importance in allowing T cells to bind to thyroid cell targets.
Keever (1993)ICAM-1T cellsExpression of LFA-1 alpha and LFA-1 beta was normal on resting cord T cells; however, they expressed significantly less ICAM-1 (CD54) than did adult PBMC.
Waldman et al. (1998)ICAM-1T cellFinally, attenuation of CMV-stimulated T cell proliferation observed in the presence of blocking Ab specific for ICAM-1 suggests a contributing role for CMV-enhanced endothelial ICAM-1 expression in the activation response.
Knight et al. (2000)intercellular adhesion molecule-1T lymphocyteAttenuation of cytomegalovirus-induced endothelial intercellular adhesion molecule-1 mRNA/protein expression and T lymphocyte adhesion by a 2'-O-methoxyethyl antisense oligonucleotide.