Viewing affirmative mentions of negative regulation of IL2 (H. sapiens) in mononuclear cells

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Elfenbein et al. (1984)interleukin-2mononuclear cellsWe found that interleukin-2 production, upon optimal stimulation, was impaired for mononuclear cells of most recipients early after marrow transplant.
Silveira-Lacerda et al. (2010)IL-2PBMCResults also showed that cis-[RuCl(2)(NH(3))(4)]Cl presents a dual role on PBMC stimulating proliferation and interleukin-2 (IL-2) production at low concentration and inducing cytotoxicity, inability to proliferate, and inhibiting IL-2 production at high concentration.
Lomnitzer et al. (1984)IL-2mononuclear cellsCon A-treated mononuclear cells (S cells) cultured with PHA-activated allogeneic or autologous responder cells showed reduced [3H]thymidine incorporation and IL-2 production as compared to activated R cells alone.
Welte et al. (1984)IL2PBMCThis study demonstrates that PBMC in patients after BMT have a defect of IL2 production but are able to express IL2 receptors in response to OKT3 antibody and to proliferate normally upon addition of hpIL2.
Siebelink et al. (1990)IL-2PBMCAlso IL-2 production levels of mitogen-activated PBMC from naturally infected symptomatic cats were significantly reduced.
Hirooka et al. (1990)interleukin-2mononuclear cellsThe present study demonstrates the usefulness of quantitating human interleukin-2 produced by human blood mononuclear cells and that there exists an impaired production of interleukin-2 in Graves' disease.
Manolagas et al. (1986)IL-2PBMThese findings support the contention that 1,25(OH)2D3-induced inhibition of PBM proliferation is mediated through selective inhibition of IL-2 production.
Lin et al. (2002)IL-2PBMCThe inhibitory mechanisms may involve the blocking of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) production, since compound 3 attenuated IL-2 and IFN-gamma production of PBMC in a dose-dependent manner.
Suthanthiran (1987)IL-2mononuclear cellsCyclosporine inhibited anti-CD3-mediated expression of IL-2 receptors and IL-2 factor production by peripheral blood mononuclear cells (PBM).
Rigby et al. (1984)IL-2mononuclear cellsFurthermore, calcitriol suppressed interleukin-2 (IL-2) production by PHA-stimulated peripheral blood mononuclear cells in a concentration-dependent fashion.
Hopkins and Failla (1997)interleukin-2mononuclear cellsAlthough dietary copper (Cu) deficiency has been associated with decreased production of interleukin-2 (IL-2) by activated splenic mononuclear cells in rodent models, the basis for this relationship and its relevance for humans remain unknown.
Hopkins and Failla (1997)IL-2mononuclear cellsFinally, incubation of human peripheral blood mononuclear cells (PBMC) with 2,3,2-tet decreased mitogen-induced IL-2 production by 50% compared with untreated controls.
Majumder and Kierszenbaum (1995)interleukin-2mononuclear cellsWe show here that the marked inhibition of interleukin-2 production seen in hosts acutely infected with Trypanosoma cruzi can be reproduced in vitro by adding a T. cruzi suspension filtrate to cultures of activated human peripheral blood mononuclear cells.
Kabuki et al. (1990)IL2mononuclear cellsSaibokuto suppressed the induction of IL2 responsiveness induced by Dermatophagoides farinae (Df) antigen in peripheral blood mononuclear cells from patients with bronchial asthma.
Kabuki et al. (1990)IL2mononuclear cellsSaibokuto suppressed the induction of IL2 responsiveness induced by Dermatophagoides farinae (Df) antigen in peripheral blood mononuclear cells from patients with bronchial asthma.
Madretsma et al. (1996)interleukin 2mononuclear cellsNicotine inhibits the in vitro production of interleukin 2 and tumour necrosis factor-alpha by human mononuclear cells.
Warren et al. (1983)IL 2PBMCThe impaired production of IL 2 by patients' PBMC may be due to this low precursor frequency.
Prync et al. (1992)Interleukin-2mononuclear cellsPilocarpine did not inhibit Interleukin-2 (IL-2) production by human peripheral blood mononuclear cells but decreased the number of interleukin-2 receptor bearing cells (TAC positive cells).
Sirota et al. (1997)IL-2CBMCIL-2 levels, tested by radioimmunoassay (RIA), were found to be reduced only in supernatants derived from CBMC of term infants and not in those derived from MC of preterm infants or adults.
Yukioka et al. (1988)interleukin-2mononuclear cellsBiological activity of 26,26,26,27,27,27-hexafluorinated analogs of vitamin D3 in inhibiting interleukin-2 production by peripheral blood mononuclear cells stimulated by phytohemagglutinin.
Akiyoshi et al. (1985)IL-2 3PBMHowever, the depressed production of IL-2 3 days after surgery could be abolished when adherent cells were removed from PBM by plastic adherence procedures.
Ford et al. (1984)Interleukin 2mononuclear cellsInterleukin 2 production by HD patients' peripheral blood mononuclear cells, however, is decreased when compared with age/sex-matched controls.
Todoroki et al. (1990)IL-2mononuclear cellsAzelastine suppressed the induction of IL-2 responsiveness induced by Df antigen in peripheral blood mononuclear cells from patients with bronchial asthma in a dose dependent manner.
Phi et al. (1989)IL-2PBMCWe suggest an intrinsic (not disease activity-related) impairment of the adenylate cyclase-dependent regulatory mechanism in the PBMC of SLE patients, which may result in a defective IL-2 production and IL-2 dependent biological functions.
Alhomsi and Laposata (2006)IL-2mononuclear cellsRESULTS: Fatty acid ethyl esters inhibited the PHA-induced IL-2 production and secretion in activated human mononuclear cells.
Alhomsi and Laposata (2006)IL-2mononuclear cellsCONCLUSIONS: Fatty acid ethyl esters inhibited PHA-stimulated IL-2 production and Ca2+ influx into human mononuclear cells and elevated intracellular cAMP concentration.
Murray et al. (1986)IL-2PBMCMean IL-2 production by PBMC in 11 melanoma patients with metastatic disease (Stage III) was significantly decreased compared with controls and was moderately decreased compared with five patients with resected nodal disease (Stage II).
Beltz and Kierszenbaum (1987)IL-2PBMCLevels of IL-2 in PHA-stimulated PBMC cultures were markedly reduced in the presence of T. cruzi.
Borzy and Ridgway (1989)IL-2PBMCIn addition, PHA-induced expression of cell-surface receptors for IL-2 on PBMC was significantly decreased in both patient groups as compared to control subjects (P less than 0.01).
Endres et al. (1993)interleukin-2mononuclear cellDietary supplementation with n-3 fatty acids suppresses interleukin-2 production and mononuclear cell proliferation.
Endres et al. (1993)Interleukin-2mononuclear cellsInterleukin-2 synthesis from stimulated peripheral blood mononuclear cells was suppressed from 6.2 ng/ml at baseline to 2.2 ng/ml 10 weeks after the end of n-3 fatty acid supplementation (65% decrease; P = .04).
Endres et al. (1993)interleukin-2mononuclear cellThe results suggest that the effect of dietary n-3 fatty acids in some diseases may be mediated in part by decreased production of interleukin-2 and decreased mononuclear cell proliferation.
Kashiwado et al. (1989)IL-2mononuclear cellsIn addition, these factors inhibited the production of IL-2 by normal human peripheral blood mononuclear cells (PBMC).
Rich et al. (1991)IL-2PBMCAM in co-culture with PBMC also inhibited PHA-stimulated IL-2 production by 70% but did not inhibit IL-2 production when AM were separated from PBMC in dual chambers.
Cereseto et al. (1999)IL-2mononuclear cellsIn N1186 cells arrested in G1 after serum/interleukin-2 (IL-2) deprivation, downregulation of the cyclin E-CDK2 kinase activity correlated with decreased phosphorylation of CDK2 and accumulation of p27Kip1 bound to the cyclin E-CDK2 complex, as seen in normal activated PBMCs (peripheral blood mononuclear cells).
Taylor et al. (1986)IL 2PBMCPHA-induced proliferation and IL 2 receptor expression peaked early in the culture period (routinely to 100,000 cpm and 50% respectively within 3 days), and colchicine did not inhibit the early induction of IL 2 receptors on PBMC.
Mansueto et al. (1997)IL-2mononuclear cellsFurthermore, a reduction in IL-2 production by peripheral blood mononuclear cells from acute BF patients was also observed. sIL-2R represents an unspecific marker useful to monitor the evolution of BF.
Krishnamurthy et al. (1995)interleukin-2PBMCThe interleukin-2 (IL-2) production by the PBMC was also significantly reduced in renal failure patients as compared to normals.
Chu et al. (1984)IL-2PBMCIL-2 production by the patient's phytohemagglutin-stimulated PBMC was severely deficient but was corrected by the addition of phorbol 12-myristate 13-acetate, suggesting a defective response to IL-1.
Tsai et al. (2008)IL-2PBMCFurthermore, seselin significantly decreased the IL-2 and IFN-gamma gene expression in PHA-activated PBMC.
Haghighi and Cathcart (1992)IL-2PBMCFactors bound and then eluted from this affinity column were shown to inhibit IL-2 production by PBMC in a manner similar to HSF.
Bunout et al. (2004)Interleukin-2PBMCInterleukin-2 production by PBMC and the proportion of T cells with NK activity decreased in controls and did not change in supplemented subjects.
Kusugami et al. (1991)Interleukin-2mononuclear cellsInterleukin-2 activity of intestinal lamina propria mononuclear cells is decreased in Crohn's disease and ulcerative colitis patients compared with control patients with noninflammatory bowel disease.
Fiedler et al. (1987)IL-2PBMCPBMC of 6 out of 7 patients with CVI studied also exhibited a profound defect in IL-2 receptor expression when incubated with OKT3 antibody.
van Dijk et al. (1998)interleukin 2mononuclear cellsTransdermal nicotine inhibits interleukin 2 synthesis by mononuclear cells derived from healthy volunteers.
van Dijk et al. (1998)IL-2mononuclear cellsCONCLUSION: The beneficial effect of transdermal nicotine in ulcerative colitis may be mediated by a selective inhibition of the IL-2 production by mucosal mononuclear cells, which could result in diminished cell proliferation and consequently a reduction in the inflammatory process.
Eisenstein et al. (1994)IL-2mononuclear cellsIL-2 production by mitogen-induced peripheral blood mononuclear cells was reported to be reduced in several autoimmune diseases, including Graves' disease (GD).
Wang et al. (1996)IL-2PBMCThe release of IL-2 and IL-6 by PHA-stimulated PBMC was significantly inhibited by titanium, chromium, and cobalt.
Lederman et al. (1995)interleukin-2mononuclear cellsProcysteine does not affect interleukin-2 production but inhibits interleukin-2 receptor expression in PHA-stimulated peripheral blood mononuclear cells.
Reed et al. (1985)IL 2PBMCAdding anti-Tac antibody to PBMC cultures to block the interaction of IL 2 with its receptor diminished the accumulation of IL 2 receptor mRNA induced by PHA.
Linker-Israeli and Casteel (1988)IL-2PBMSF PBM appear to affect directly the IL-2 producer cell, since it suppressed IL-2 production by (1) mitogen stimulated PBM depleted of CD8+ suppressor cells and by (2) mitogen induced Jurkat cells.
Russwurm et al. (2002)IL-2PBMCMild hyperthermia significantly impaired IL-2 gene expression in PHA-stimulated cultures of PBMC and decreased IL-2 release in all variants of cultures.
Pullman and Doe (1992)IL-2LPMCLPMC IL-2 production was markedly suppressed by drugs used in IBD therapy. 5-Aminosalicylic acid (5-ASA) reduced activity in a dose-dependent fashion.
Pullman and Doe (1992)IL-2LPMCAt a dose equivalent to the faecal therapeutic level of 0.5 mg/ml activity, IL-2 production by LPMC was suppressed to 3.4% of controls.
Pullman and Doe (1992)IL-2LPMCSimilarly, exposure of LPMC to cyclosporin A (CyA) and hydrocortisone (HC) at therapeutic levels reduced IL-2 activity to less than 1% of controls.
Wu et al. (2007)IL-2PBMCWe suggested that the inhibitory effects of tanshinlactone A on PHA-induced PBMC proliferation, appeared to be mediated, at least in part, through reduction of MAPK activation and IL-2 and IFN-gamma production.
Zhang et al. (2002)IL-2mononuclear cellsAlthough functional studies have mostly demonstrated decreased in vitro production of IL-2 by peripheral blood mononuclear cells (PBMCs) stimulated with mitogen, the reason is unclear.
Ihenetu et al. (2003)interleukin 2mononuclear cellsPharmacological characterisation of cannabinoid receptors inhibiting interleukin 2 release from human peripheral blood mononuclear cells.
Mullen et al. (2007)IL-2PBMCThis study showed that CLA supplementation reduced PBMC IL-2 secretion from Con A-stimulated PBMC but lacked effect on other markers of the human inflammatory response.
Linker-Israeli et al. (1985)IL-2mononuclear cellThese studies suggest that one or more circulating mononuclear cell subsets in SLE patients can suppress IL-2 production and that one subset may possibly belong to a non-T, non-B "third mononuclear population."
Lakhanpal and Handwerger (1987)IL2PBMSome patients with SLE have a defect in rIL2-induced proliferation of their "resting" PBM that seems unrelated to a concomitant defect in phytohemagglutinin-induced IL2 receptor acquisition.
Atluru et al. (1991)interleukin-2mononuclear cellsGenistein, a selective protein tyrosine kinase inhibitor, inhibits interleukin-2 and leukotriene B4 production from human mononuclear cells.
Atluru et al. (1991)interleukin-2PBMCIn this study, genistein, a selective protein tyrosine kinase (PTK) inhibitor, inhibited peripheral blood mononuclear cell (PBMC) proliferation and interleukin-2 production from cultures that were stimulated with phytohemagglutinin (PHA), phorbol 12-myristate 13-acetate (PMA) plus A23187, or PHA plus PMA, and genistein effectively blocked the PHA plus IL-2-induced PBMC proliferation.
Nakayama et al. (1983)TCGFmononuclear cellsDecreased TCGF activity in the culture medium of PHA stimulated peripheral mononuclear cells from patients with metastatic cancer.
Blasco et al. (1995)IL-2PBMCJacalin-CD4 interaction and the proliferation of PBMC, as well as IL-2 secretion by Jurkat cells were inhibited by specific jacalin-competitive sugars.
Chin et al. (1986)interleukin 2WMCIn contrast, lymphokine (i.e., interleukin 2)-activated killer (LAK) cytotoxicity is not deficient in cord WMC.
Weir et al. (1991)IL-2mononuclear cellThe 5-LO does not inhibit mononuclear cell responses simply by shunting the formation of arachidonic acid precursors to form inhibitory prostaglandins, since it does not impair IL-2 responsiveness in a manner similar to ENO.
Deacock et al. (1992)interleukin-2mononuclear cellsA limiting dilution analysis (LDA) has been established which measures the total numbers of alloreactive interleukin-2 (IL-2)-secreting T cells in human peripheral blood mononuclear cells (PBMC).
Cooley et al. (1989)IL2PBMCStatistical analysis of the clinical factors possibly affecting lymphokine synthesis showed that in vivo cyclosporin A did not affect the in vitro capacity of PBMC to produce cytokines, although steroid therapy had a negative effect on IL2 production.
Carlsson et al. (1987)interleukin 2mononuclear cellsHuman mononuclear cells stimulated with staphylococcal enterotoxin A (SEA) for 2-6 days significantly suppress [3H]thymidine incorporation and reduce the levels of interleukin 2 (IL-2) and interferon (IFN) in culture medium when added to fresh, polyclonally activated mononuclear cells.
Di Renzo et al. (1997)IL2PBMCBesides, they showed a significantly reduced PBMC IL2 production, which was evaluated both through an ELISA method and a biological assay.
Linker-Israeli et al. (1988)IL-2PBMIL-2 production by peripheral blood mononuclear cells (PBM) is decreased in patients with systemic lupus erythematosus (SLE).
Linker-Israeli et al. (1988)IL-2PBMThe CD8- CD16+ non-T cell subset suppressed IL-2 production by normal and SLE PBM in autologous and allogeneic combinations.
Matsubayashi et al. (1991)IL-2mononuclear cellsSoluble IL-2 receptor (sIL-2R) in supernatants of peripheral mononuclear cells stimulated by IL-2 from these patients also was measured.
Romagnani et al. (1985)IL2mononuclear cellsHowever, crude supernatants from protein A-stimulated peripheral blood mononuclear cells, which were found to possess both IL2 and B cell growth factor (BCGF) activities, maintained the ability to promote proliferation of anti-mu-activated B cells after depletion of IL2.
Hollander and Elson (1990)IL-2SFMIt is concluded that an IL-2 inhibitor in RA SF is unlikely to be the cause of SFM hyporesponsiveness to mitogens.
Draeger et al. (1986)IL-2MNCTo study IL-2 responsiveness, proliferation of MNC was studied under conditions where endogenous IL-2 production is limiting.
Briggs et al. (1999)IL-2PBMCAs expected, cyclosporine was significantly more suppressive than either glucocorticoid of IL-2 mRNA expression and IL-2 production by mitogen-stimulated PBMC, with variable degrees of inhibition in cells from individual subjects.
Donnelly et al. (1986)IL-2PBMCCoculture of PBMC with NPT-15392 and concanavalin A (Con A) for 24 h resulted in significant increase of IL-2 in the supernatants of such cultures as compared with the IL-2 levels of control, non-NPT-treated, Con A-activated cultures.
Suzuki et al. (1984)IL-2mononuclear cellsThis potentiation of IL-2 on NK enhancement was suppressed by PGE2, and was enhanced by indomethacin in the experiments using unfractionated mononuclear cells.
Dohlsten et al. (1986)interleukin 2mononuclear cellsHistamine, a modulator of various immune functions, inhibits the production of interleukin 2 (IL-2) and interferon-gamma (IFN-gamma) by polyclonally activated human blood mononuclear cells.
Huchet and Grandjon (1988)IL-2mononuclear cellsHistamine at molar concentrations ranging from 10(-5) to 10(-7) exerted an inhibitory effect upon IL-2 synthesis by peripheral blood mononuclear cells in normal man; two pathways of inhibition are described.
Lin et al. (2000)interleukin-2HMNCThe inhibitory mechanisms may involve the blocking of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) production, since VC-ME suppressed IL-2 and IFN-gamma production of HMNC in a dose-dependent manner.
Trifiletti et al. (1989)IL2PBMCThe addition of autologous E significantly depressed IL2 levels in PWM-stimulated PBMC cultures.
Piccolella et al. (1986)interleukin-2mononuclear cellsDexamethasone inhibits the expression of the interleukin-2 receptor, the synthesis of immune interferon, and the development of natural killer cells when added to peripheral blood mononuclear cells cultured with soluble microbial antigens (purified protein derivative and a polysaccharide extract from Candida albicans [MPPS]) or human recombinant interleukin-2.