◀ Back to IL2

ICAM1 — IL2

Text-mined interactions from Literome

Sindhi et al., J Immunol Methods 2003 : PD analyses suggested that in NHS samples containing CsA+SRL ( n=5 ), ( 1 ) PMA-Ionomycin stimulated T-cell expression of intracellular IL-2 , TNF-alpha, and IFN-gamma was inhibited by CsA, and minimally by SRL, and ( 2 ) the two agents inhibited pokeweed mitogen ( PWM ) -stimulated B-cell expression of CD54 and CD95, but not CD86 ( ICAM-1, Fas antigen, and B7.2 ), synergistically
Triozzi et al., Cell Immunol 1992 (Carcinoma, Renal Cell...) : IL-2 induction of ICAM-1 and the maintenance of CD18 complex expression on small lymphocytes separated by Percoll gradients were similar to that on LGL ... We conclude that IL-2 enhances the expression of ICAM-1 on multiple human lymphocyte populations including LGL effectors
Giavazzi et al., Cancer Res 1992 (Melanoma) : Tumor necrosis factor, interleukin 1, and gamma-interferon also caused the release of soluble ICAM-1
Andersen et al., Nephrol Dial Transplant 1992 : Furthermore, the in vitro model indicates that ICAM-1 expression is regulated by gamma-interferon and interleukin-1 produced by activated T lymphocytes and macrophages
Stuyt et al., Immunology 2003 : Selective regulation of intercellular adhesion molecule-1 expression by interleukin-18 and interleukin-12 on human monocytes
Moreira et al., Am J Pathol 2006 (Disease Susceptibility...) : Expression of ICAM-1 was up-regulated on T lymphocytes after infection with the fungus, and its expression was dependent on interferon-gamma, tumor necrosis factor-alpha, and interleukin-12
Olive et al., J Immunother (1991) 1991 (Leukemia, Myeloid, Acute) : We found that, in three of five patients, IL-2 could induce , in vivo, an increase in the expression of CD54/ICAM-1 and to a lesser extent of CD58/LFA-3 on bone marrow leukemic blasts
Schoen et al., Nutrition 2009 (Inflammation) : Furthermore, activation of natural killer cell cytotoxicity in response to interleukin-2 stimulation ( P < 0.05 ), a reduction of total lipid peroxidation, and a reduction of soluble vascular cell adhesion molecule-1 ( P < 0.01 ) and soluble intercellular adhesion molecule-1 ( P < 0.05 ) as inflammatory blood markers were found in the Regulat but not in the placebo group
Van Seventer et al., J Immunol 1990 : The proliferative response to co-immobilized OKT3 and ICAM-1 is dependent on the IL-2R , which is induced only in the presence of both OKT3 and ICAM-1
Krutmann et al., J Invest Dermatol 1990 : Stimulation of cells with recombinant human ( rh ) interleukin (IL) 1 alpha, rhIL-4, rhIL-5, rhIL-6, rh granulocyte/macrophage colony stimulating factor ( GM-CSF ), rh interferon alpha ( rhIFN alpha ), and rh transforming growth factor beta ( TGF beta ) did not increase ICAM-1 surface expression
Giwa et al., Neurology 2012 (Cerebral Small Vessel Diseases) : Endothelial dysfunction is a possible causal factor, and circulating markers of endothelial activation ( intercellular adhesion molecule-1 , thrombomodulin ) and inflammation ( interleukin [ IL]-6 ) are elevated in patients with SVD
Poudrier et al., J Exp Med 1994 : Strikingly, cross linking ligation of CD54 and MHC II in the presence of IL-5 induced expression of a functional IL-2R on small resting B cells
Hathorn et al., Cancer 1994 (Carcinoma, Renal Cell...) : Exogenous IL-2 and/or IFN-alpha treatment of a IFN-alpha-resistant RCC enhanced both HLA class I antigen and ICAM-1 expression and suppressed CD44 expression, but had no effect on tumor growth rate
Sano et al., Mol Cell Biochem 1994 : Cellular expression of ICAM-1 was drastically induced by TNF or interleukin-1 stimulation, and the moderate expression with delayed-action was observed only by lipopolysaccharide stimulation
Wake et al., Blood 1995 (Bone Resorption...) : We 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
Boussiotis et al., J Exp Med 1993 : Although equivalent in their ability to costimulate maximal proliferation of alloreactive T cells, B7 but not ICAM-1 induced detectable interleukin 2 secretion and prevented the induction of alloantigen-specific anergy
Campbell et al., J Urol 1994 (Carcinoma, Transitional Cell...) : In contrast, interleukin-1 and phorbol myristate acetate exhibited variable effects on ICAM-1 expression, and interferon-alpha had no effect
Shrikant et al., J Neuroimmunol 1994 (Encephalomyelitis, Autoimmune, Experimental) : Regulation of intercellular adhesion molecule-1 gene expression by tumor necrosis factor-alpha, interleukin-1 beta, and interferon-gamma in astrocytes
Dummer et al., Dermatology 1994 (Leukemia, Erythroblastic, Acute...) : In the SeAx line, IL-2 and IFN-gamma inhibited ICAM-1 release
Czech et al., J Invest Dermatol 1993 (Hypersensitivity, Immediate) : Cytokine induced ICAM-1 expression was specific, because IL-1 alpha, IL-1 beta, IL-2 , IL-4, IL-6, IL-7, IL-8, C5a, and platelet activating factor did not significantly affect eosinophil ICAM-1 surface expression
Alileche et al., Oncogene 1993 (Melanoma) : In M14 cells, recombinant IL2 ( 36 pM ) induces the down modulation of ICAM-1 expression at the surface of M14 cells
Plaisance et al., Int Immunol 1993 : IL-2 induction of ICAM-1 was only observed in sparse cultures and for IL-2 concentrations over 180 pM
Deisher et al., Life Sci 1993 (Second Messenger Systems) : Surface protein expression of vascular cell adhesion molecule-1, endothelial leukocyte adhesion molecule-1, or intercellular adhesion molecule-1 , which is induced by tumor necrosis factor, interleukin-1 , and lipopolysaccharide, was not induced by pentoxyfilline, a phosphodiesterase inhibitor, nor by dibutyryl cyclic adenosine monophosphate
Lai et al., Int J Cancer 1993 (Fibrocystic Breast Disease) : Possible regulation of soluble ICAM-1 levels by interleukin-1 in a sub-set of breast cysts
Mäenpää et al., Int J Cancer 1993 : CD2, CD44, CD54 and CD58 were increased by IL-2 but L-selectin was strongly down-regulated on the long-term activated NK cells
Rabinovici et al., Circ Res 1996 : Furthermore, TNF-alpha inhibition prevented the upregulation of lung tissue IL-1 beta, IL-6, cytokine induced neutrophil chemoattractant, and E-selectin ( ELAM-1 ) but not intercellular adhesion molecule-1 mRNAs in response to IL-2
Baumgartner-Parzer et al., Diabetologia 1995 : Stimulation of confluent HUVECs, kept in 30 vs 5 mmol/l glucose for 13 +/- 1 days, with 20 U/ml interleukin-1 for 24 h ( ICAM-1 ) and 4 h ( endothelial leukocyte adhesion molecule 1 ) resulted in reduced ICAM-1 ( 84.8 +/- 27.0 %, p < 0.05 ) and endothelial leukocyte adhesion molecule-1 ( 87.6 +/- 22.4 %, p < 0.05 ) expression vs control cells, while that of PECAM ( t : 24 h ) and vascular cell adhesion molecule-1 ( t : 16 h ) remained unchanged
Perretti et al., Biochem Biophys Res Commun 1996 : This opposite modulatory role of interleukin-1 and dexamethasone on intercellular adhesion molecule-1 expression was also, for the first time, observed in vivo using mouse peritoneal macrophages : a four-fold increase in intercellular adhesion molecule-1 expression was measured after local administration of the cytokine ( 5 micrograms/kg ) and this effect was greatly inhibited ( > 70 % ) by co-injection with 1 microgram dexamethasone
Ikeda et al., J Am Soc Nephrol 1996 : In an enzyme linked immunosorbent assay, interleukin 1 beta ( IL-1 beta ; 10 ng/mL ) increased ICAM-1 molecule expression on cultured rat mesangial cell surface in a time dependent manner
Zuckerman et al., J Immunol 1998 : Nevertheless, coexpression of ICAM-1 or B7-1 on ProAd is required to induce detectable levels of IL-2 gene expression in either Th1 clones or naive T cells ... In Th1 clones, activation by ProAd-ICAM induces very transient IL-2 mRNA expression that does not result in detectable IL-2 secretion or T cell proliferation
Wang et al., Circ Res 1998 : Cardiac graft intercellular adhesion molecule-1 ( ICAM-1 ) and interleukin-1 expression mediate primary isograft failure and induction of ICAM-1 in organs remote from the site of transplantation
Labuda et al., Immunology 1998 : ICAM-1 costimulation induces IL-2 but inhibits IL-10 production in superantigen activated human CD4+ T cells ... The ICAM-1 induced IL-2 production could efficiently be abrogated with monoclonal antibody ( mAb ) against ICAM-1 or LFA-1, showing that the activation is dependent of a functional ICAM-1-LFA-1 pathway
Deeths et al., Eur J Immunol 1999 : ICAM-1 also synergizes with B7-1 for the induction of IL-2 production in CD8+ but not CD4+ T cells