Viewing negative mentions of positive regulation of IL2 (H. sapiens) in lymphocytes

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Medveczky et al. (1993)interleukin-2lymphocytesWe show in this report that infection of human peripheral white blood cells with a group C strain 484-77 results in selective expansion of CD8 lymphocytes with strong cytotoxic activity and these cells do not require interleukin-2 (IL-2) for growth.
Kubbies et al. (1990)IL2lymphocytesUsing a novel flow cytometric assay (BrdU/Hoechst flow cytometry) for the visualization and quantitation of cell activation and cell progression through multiple cell cycles we show that (1) resting mononuclear cells from human venous blood respond to polyclonal activation in a highly asynchronous fashion, as some of these cells enter their first cell cycle as early as 30 and as late as 80 hrs after exposure to the mitogen; (2) reducing agents improve the mitogenic response of polyclonally activated human lymphocytes by increasing the recruitment of non-cycling G0/G1 cells; (3) of 8 reducing agents tested, alpha-thioglycerol proved most effective with respect to enhancing recruitment into the cell cycle; (4) the effective agents needs to be present permanently for maximum response; (5) the growth-promoting effect of alpha-thioglycerol is mediated, but not solely caused by increased IL2 production.
Roffman et al. (1984)interleukin 2lymphocytesChemical reduction of oxidized human lymphocytes inhibits interleukin 2 production but not induction of interleukin 2 responsiveness.
Hirano et al. (1984)IL 2lymphocytesTPA alone did not induce the production of IL 2 in human tonsillar lymphocytes but enhanced the PHA-induced IL 2 production by seven-fold.
Morioka et al. (1993)IL-2PBLF4 enhanced IL-2-induced proliferation and IL-2 receptor (Tac) expression of PBL without significant increase of IL-2 production.
Yamamoto et al. (1986)IL2 mRNAlymphocytesAddition of alpha-methylornithine and methylglyoxal bis (guanyl hydrazone), which inhibit polyamine synthesis, did not affect the induction of IL2 mRNA in the lymphocytes stimulated with PHA and TPA, indicating that polyamine synthesis is not necessary for IL2 mRNA induction.
Langkamp-Henken et al. (2000)interleukin 2lymphocyteCONCLUSIONS: Pharmacologic doses of arginine were well tolerated but did not enhance lymphocyte proliferation or interleukin 2 production in nursing home residents with pressure ulcers.
Blank et al. (1987)IL-2lymphocyteTrophoblast was demonstrated to be unable to cause the production of interleukin-2 (IL-2) by allogeneic splenocytes in vitro in two ways: 1) The addition of lymphocyte-trophoblast culture-supernatant (LTC-SN) did not stimulate the proliferation of IL-2 dependent cytotoxic T lymphocyte (CTL-L cells; 2) When responder cells were cultured with heat-treated splenocytes (usually no CTL generation) an increase of CTL formation could be seen in the presence of mixed lymphocyte culture-supernatant (MLC-SN) but not of SN from the cultures in which trophoblast cells served as stimulators.
Keicho et al. (1993)IL-2lymphocytesEM had a suppressive effect on the proliferative response of human lymphocytes stimulated with mitogens and antigens, while EM had no effect on concanavalin A (Con A)-induced interleukin-2 (IL-2) production or IL-2R alpha (CD25) expression.
Mansfield et al. (1991)IL-2TILsThey also failed to induce IL-2 production in uncultured TILs, although anti-CD3 mAb, but not HC antibody, stimulated IL-2 production in peripheral blood mononuclear cells (PBMCs).
Slauson et al. (1984)IL-2lymphocyteSerotonin thus produced an inhibition of lectin-stimulated lymphocyte proliferation via a mechanism independent of IL-2 production, and caused a decrease in the expression and distribution of IL-2 receptors on the surface of responder cells.
Noma et al. (1985)IL 2lymphocyteFurthermore, these populations produced relatively pure interleukin 2 (IL 2) by stimulation of an autologous mixed lymphocyte reaction without any absorption of IL 2 produced in the same culture.
Yamamoto et al. (1986)IL2 mRNAlymphocytesHowever, the lymphocytes cultured with dibutyryl cAMP or dibutyryl cGMP could not be activated to produce IL2 mRNA.
Shiratsuchi et al. (1987)IL-2PBLA further characterization of this low responsiveness to PPD revealed that PBL from these advanced tuberculous patients failed to generate interleukin-2 (IL-2) in response to PPD stimulation.
Kozenitzky et al. (1992)IL-2lymphocyteIn the present study, the addition of AS101 and PMA serve to restore the impaired IL-2 production, T- and T-helper lymphocyte functional activity, but not the IL-2R release.
Kawano et al. (1992)IL2lymphocytesHowever, the CD45RA antibody pretreatment gave rise to Df-induced IL2 responsiveness in the lymphocytes of the patients sensitized with OVA but not with Df; conversely, OVA-induced IL2 responsiveness was enhanced in Df- but not in OVA-sensitized lymphocytes.
Wigfall et al. (1988)IL-2PBLThere was no significant increase in IL-2 receptors expression in PBL from active SLE patients in response to mitogenic stimulation with PHA compared to inactive SLE patients and normal donors.
Sharom et al. (1990)Interleukin-2lymphocytesInterleukin-2 (IL-2) production by ganglioside- and glycophorin-treated lymphocytes was unchanged.
Thoman et al. (1984)IL 2lymphocyteIn addition, synthesis of IL 2 in mixed lymphocyte cultures is blocked by C3d-K, but not IL 2 synthesis induced by Con A.
Hauser et al. (1987)IL-2lymphocytesThese results suggest that the proposed defect in cellular immunity during pregnancy is not mediated by an inability of the lymphocytes to produce IL-2.
Viret et al. (1995)IL-2lymphocytesTogether these data suggest that defective IL-2 secretion by many tumour-infiltrating lymphocytes clones in response to antigen presentation by melanoma cells in vitro is not exclusively due to the inability of these cells to provide an appropriate co-stimulation through the B7-1 molecule.
Emara and Carroll (1992)IL-2PBLsHowever, crosslinking CD7 and/or FcRmu of PBLs significantly reduced phytohemagglutinin (PHA)-induced IL-2 production and rendered PBLs unable to utilize exogenously added human recombinant IL-2 (rIL-2).
Uberti et al. (1994)IL-2PBLIncreasing the IL-2 concentrations beyond 600 IU/ml did not augment the proliferative or cytotoxic responses of PBL.
Loertscher et al. (1987)IL-2lymphocytesWe conclude that metabolically compromised lymphocytes activate Ts and are sufficient to stimulate IL-1 and IL-3 synthesis but do not transmit an unknown signal required for the activation of IL-2 synthesis and IL-2 receptor expression on a yet-to-be-defined T cell subset.
Linker-Israeli et al. (1985)IL-2lymphocytesThree lines of evidence suggest that the SLE OKT8+ cells actively inhibit the production of IL-2 rather than passively absorb this lymphokine: (a) only 3.2% of SLE lymphocytes expressed IL-2 receptors as detected with anti-Tac; (b) freshly prepared SLE lymphocytes did not absorb IL-2; and (c) cell-free supernatants from SLE OKT8+ cells inhibited IL-2 production, but not IL-2 activity.
Simpson et al. (1983)lymphokinelymphocytesThese results suggest that leucocyte migration inhibition by gluten in coeliac disease is not due to lymphokine production by sensitised lymphocytes but is caused by cytophilic antibody.
Kradin et al. (1989)IL-2PBLLectin stimulation of PBL produced little IL-2 secretion during treatment, while IFN-gamma secretion persisted.
Mudido et al. (1996)interleukin 2-inducedlymphocytesThere was no increase in spontaneous or interleukin 2-induced lymphocyte proliferation or p24 antigen production by patients' lymphocytes that were examined immediately after blood transfusion.
Redelman and Wormsley (1986)TCGFlymphocyteTherefore, it appears that the initial expression of TCGF receptors detected after lymphocyte activation does not require de novo production of RNA.
Sharma et al. (1984)interleukin 2PBLEnhancement of NK activity by PBL incubated with Toxoplasma sonicate was accompanied by a concomitant increase in interferon (IFN), but not of interleukin 2 (IL-2), levels in supernatants of the cell cultures.
Sfikakis et al. (1998)IL-2 mRNAlymphocytesIn contrast, 2-CdA (0.1 microgram/ml) at concentrations that inhibit by 80-90% the PHA-induced proliferative responses of lymphocytes did not affect IL-2 mRNA accumulation.
Goodwin et al. (1986)IL-2lymphocyteThus, endogenous LTB4 production appears to be necessary but not sufficient for phytohemagglutinin-induced IL-2 production and lymphocyte proliferation.
Carlsson et al. (1987)IL-2lymphocyteThe collective data show that the SEA-induced suppression of IL-2 activity in lymphocyte culture medium is not due to a suppression of the IL-2 production but rather depends on depletion of IL-2 due to absorption of IL-2 from the culture medium.
Divine et al. (1988)IL2lymphocyteAs normal, patient CD8 lymphocytes do not suppress (1) phytohemagglutinin (PHA)-induced interleukin 2 (IL2) receptor expression and IL2 responsiveness by normal T cells or (2) the mixed lymphocyte reaction of donor cells.
Beno et al. (1995)IL-2lymphocytesGeneration of the antifungal lymphocytes in culture required IL-2 and was not replaced with IFN-gamma.
Summerfield and Saalmüller (1998)interleukin-2lymphocyteIn vitro analysis of the influence on the lymphocyte function demonstrated neither an increase of the immunoglobulin synthesis, nor of the interleukin-2 production, nor of the cytolytic activities.
Heemskerk et al. (2008)IL-2TILsIn this study, insertion of the IL-2 gene into antitumor TILs increased their ability to survive after IL-2 withdrawal in vitro but did not increase their in vivo persistence or clinical effectiveness.
Takahashi et al. (1997)IL-2lymphocytesThe low IL-2 producing activity of their PBMC and lymphocytes against anti-CD3 MoAb could not be overcome by stimulation with phorbol myristate acetate and ionomycin.
Koliaskina et al. (2007)interleukin-2lymphocytesThe functional activity of immunocompetent cells (the phagocyte activity of neutrophiles and monocytes, the cytotoxic activity of natural killer lymphocytes, interleukin-2, and interleukin-10 production) did not depend on the clinical condition of the patients and the therapy and was significantly lower than that of controls both before and during the treatment.
Schönfeld and Zahner (2000)interleukin 2lymphocytesProliferative responses of spleen lymphocytes to concanavalin A (Con A) and lipopolysaccharides (LPS), but not Con-A-induced interleukin 2 (IL-2) production, were found to be suppressed in infected animals during patency as compared with uninfected controls.
Bierer et al. (1988)IL-2lymphocyteHowever, liposomes containing both purified LFA-3 and HLA-DR, the physiological ligands for CD2 and the TCR, respectively, stimulate IL-2 production by the CD2+ but not the parent hybridoma, suggesting that complementary interactions between the TCR-CD3 complex and the CD2 pathway may regulate lymphocyte activation.
Groenewegen et al. (1985)lymphokinelymphocytesIt is concluded that CsA inhibits the production of an MHC class-II-antigen-inducing lymphokine produced by lymphocytes in mixed cultures; allogeneic stimulation is not necessary for production of the lymphokine.
Barnes et al. (1992)IL-2lymphocytesIn contrast, LAM did not induce transcription of mRNA for cytokines produced predominantly by lymphocytes, such as lymphotoxin, IFN-gamma, IL-2, IL-3, or IL-4.
Rall et al. (1996)IL-2lymphocyteTraining did not induce changes in PBMC subsets, interleukin (IL)-1 beta, tumor necrosis factor-alpha (TNF), IL-6, IL-2, or PGE2 production, lymphocyte proliferation, or DTH response in any of the training groups, compared with control subjects.
Touraine (1989)IL-2lymphocytesIL-2 production was increased in Con A-activated but not in resting lymphocytes.
Chatila et al. (1989)interleukin-2lymphocyteThe patient's circulating lymphocytes were normal in number and phenotype, but stimulation of the T-cell receptor by antigens, mitogens, and monoclonal antibodies failed to induce interleukin-2-receptor expression, interleukin-2 synthesis, or lymphocyte proliferation.
Frieboes et al. (1999)interleukin-2lymphocyteUnder PAN treatment, tumor necrosis factor (TNF)-alpha, soluble TNF receptors p55 and p75, and soluble interleukin-2 receptor levels were not increased and neither were monocyte and lymphocyte counts affected.
Ho et al. (1995)interleukin-2lymphocyteIn vivo CD3+CD25+ lymphocyte subpopulation is down-regulated without increased serum-soluble interleukin-2 receptor (sIL-2R) by gonadotropin releasing hormone agonist (GnRH-a).
Chi et al. (2005)IL-2lymphocytesBut no rise of IL-2 and TNF-gamma was found. (3) The proliferated cells were mainly CD4+ lymphocytes.
Nair et al. (2004)IL-2lymphocytesImmune activation by RR1 in normal lymphocytes elicited the synthesis of interleukin (IL)-1beta (1080 pg/ml), IL-6 (21,833 pg/ml), IL-12 p70 (50.19 pg/ml), IL-12 p40 (918.23 pg/ml), IL-18 (27.47 pg/ml), IFN- gamma (90.16 pg/ml), tumor necrosis factor (TNF)-alpha (2225 pg/ml) and monocyte chemoattractant protein (MCP)-1 (2307 pg/ml) at 100 microg/ml concentration, while it did not induce the production of IL-2, IL-4, IL-10, interferon (IFN)-alpha and TNF-beta.