| Document |
Target |
Regulator |
Anatomy |
Sentence |
| Horst and Flad (1987) | interleukin 2 | | | Corticosteroid-interleukin 2 interactions: inhibition of binding of interleukin 2 to interleukin 2 receptors.
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| Plitnick et al. (2001) | interleukin-2 | IL-2 | | Lipoteichoic acid inhibits interleukin-2 (IL-2) function by direct binding to IL-2.
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| Moreau et al. (1995) | IL-2 | | | Characterization of a monoclonal antibody directed against the NH2 terminal area of interleukin-2 (IL-2) and inhibiting specifically the binding of IL-2 to IL-2 receptor beta chain (IL-2R beta).
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| Nicholas et al. (1984) | interleukin-2 | Human pregnancy serum | | Human pregnancy serum inhibits interleukin-2 production.
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| Bruserud and Lundin (1987) | Interleukin 2 | Warfarin | | Warfarin inhibited Interleukin 2 (IL-2) production, but had only minimal effects on expression of IL-2 receptors or IL-2 dependent proliferation. |
| Lillehoj and Shevach (1985) | IL-2 | CsA | T cells | In contrast, CsA blocked acquisition of responsiveness of resting T cells to IL-2, inhibited IL-2 production, and also inhibited IL-2 receptor expression at 48 hrs but not at 24 hrs following mitogen stimulation. |
| Santoli and Zurier (1989) | IL-2 | AA | | Time course experiments showed that DGLA and AA inhibited IL-2 production even at times of minimal or no PGE release by the treated cultures. |
| Theander et al. (1988) | IL-2 | | lymphocytes | Furthermore, treatment of phytohemagglutinin-stimulated lymphocytes with AP and ELA resulted in inhibition of binding of intact IL-2 to IL-2 receptors on the stimulated lymphocytes. |
| Schmidt et al. (1990) | interleukin-2 | Cyclosporin A (CsA) | T-cell | Cyclosporin A (CsA) is thought to exert its immunosuppressive effects by inhibiting the expression of a distinct set of lymphokine genes which are induced upon T-cell activation, among them the gene coding for interleukin-2. |
| Ranjan et al. (2004) | IL-2 | Curcumin | SP-L | Curcumin inhibited IL-2 synthesis in Con A, PHA, and PMA stimulated SP-L in a concentration-dependent manner with an ED50 (concentration required for 50% inhibition) measured at 3.5 microg/ml. |
| Fox et al. (1994) | interleukin 2 | cell | T cell | Inhibition of interleukin 2 production and alteration of interleukin 2 mRNA processing by human T-T cell hybridoma-derived suppressor factors.
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| Yeh et al. (1984) | TCGF | Anti-Tac antibody | thymocytes | Anti-Tac antibody (10(-3)) inhibited the expression of TCGF receptors and late proliferation of thymocytes. |
| Haghighi and Cathcart (1992) | IL-2 | HSF | mononuclear cells | Hybridoma suppressor factor(s) (HSF), secreted by a human thymus hybridoma (8E-24) established in this laboratory, suppresses Ig as well as IL-2 synthesis by peripheral blood mononuclear cells (PBMC). |
| Dao et al. (1993) | IL-2 | IFN-alpha | MOLT-14 | In addition, the IL-2 production by PHA-stimulated MOLT-13 and MOLT-14 cells was also augmented by human natural tumor necrosis factor-alpha (TNF-alpha) in a dose-dependent manner but was inhibited by IFN-alpha even at low concentrations (10 IU/ml). |
| Wang et al. (1990) | IL-2 | TDSF | lymphocytes | The results showed that TDSF was able to markedly inhibit the production of IL-2 from PHA-stimulated lymphocytes and IL-2-dependent proliferation of activated lymphocytes, and to partially inhibit the expression of IL-2 receptor. |
| Colquhoun et al. (1993) | IL-2 | IL-4 | lymphocytes | IL-4 inhibits IL-2 induction of LAK cytotoxicity in lymphocytes from a variety of lymphoid tissues.
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| Baine et al. (1995) | IL-2 | WIN 53071 | | WIN 53071 inhibited IL-2 production induced in the calcium-dependent PMA and ionomycin pathway. |
| Ren et al. (2008) | IL-2 | collutellin A | | Inhibition of IL-2 production by collutellin A at such a low concentration indicates the potential immunosuppressive activity of this compound. |
| Pockley and Bolton (1989) | interleukin-2 | PP14 | lymphocytes | Placental protein 14 (PP14) inhibits the synthesis of interleukin-2 and the release of soluble interleukin-2 receptors from phytohaemagglutinin-stimulated lymphocytes.
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| Pockley and Bolton (1989) | IL-2 | PP14 | lymphocytes | These results suggest that PP14 inhibits the production of IL-2 from mitogenically stimulated lymphocytes, and leads to a reduced IL-2R release. |
| Elliott et al. (1992) | interleukin-2 | GSF | T-cells | GSF also inhibits production of interleukin-2 (IL-2) by mitogen activated human T-cells. |
| Murakami et al. (1988) | IL2 | HSF | HSF | Human hybridoma suppressor factor (HSF) inhibits IL2 production in addition to suppressing immunoglobulin production.
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| Murakami et al. (1988) | IL2 | HSF | HSF | These results suggest that HSF in the presence of monocytes modulates the function of T4+ cells by inhibiting IL2 production. |
| Murakami et al. (1988) | IL2 | HSF | HSF | The inhibition of IL2 production by HSF appears to be responsible for the suppression of antibody production.
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| Tomita et al. (1990) | IL-2 mRNA | HSF | HSF | This evidence was further supported by experiments in which HSF selectively suppressed the accumulation of IL-2 mRNA without affecting IL-2R (p55) mRNA expression in mitogen-stimulated PBMC. |
| Chouaib and Fradelizi (1982) | IL2 | | T lymphocytes | We have observed that a complete depletion of adherent monocytes abrogates IL2 production by T lymphocytes. |
| Chouaib and Fradelizi (1982) | IL2 | | monocytes | On the other hands in humane inhibition of IL2 production was also mediated by an excess of monocytes. |
| Chouaib and Fradelizi (1982) | IL2 | | T cell | These results suggest that activation of a radiosensitive T cell by monokines is required for the inhibition of IL2 production. |
| Bettens et al. (1984) | interleukin 2 | | T lymphocytes | Lymphokine regulation of human lymphocyte proliferation: formation of resting G0 cells by removal of interleukin 2 in cultures of proliferating T lymphocytes.
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| Ghoneum et al. (1987) | Interleukin-2 | | | Interleukin-2 and lymphotoxin production were decreased by 64% and 38%, respectively. |
| Elfenbein et al. (1984) | interleukin-2 | | mononuclear cells | We found that interleukin-2 production, upon optimal stimulation, was impaired for mononuclear cells of most recipients early after marrow transplant. |
| Elfenbein et al. (1984) | interleukin-2 | | | There appear to be defects in both interleukin-2 production and interleukin-2 responsiveness in this system early after marrow transplant.
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| Silveira-Lacerda et al. (2010) | IL-2 | | PBMC | Results 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. |
| Katsiari and Tsokos (2006) | interleukin-2 | | | Transcriptional repression of interleukin-2 in human systemic lupus erythematosus.
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| Katsiari and Tsokos (2006) | IL-2 | | T cells | T cells from patients with SLE produce decreased amounts of interleukin-2 (IL-2), a central cytokine in the regulation of the immune response. |
| Katsiari and Tsokos (2006) | IL-2 | | T cells | We discuss herein the abnormalities underlying IL-2 deficiency in SLE T cells.
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| Petrov and Lijnen (2000) | IL-2 | | | The normal expression of IL-2 receptors was preserved while the IL-2 production was blocked in the presence of nifedipine or mibefradil.
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| Williams et al. (1996) | IL-2 | | T cell | DGLA suppresses T cell activation and production of interleukin-2 (IL-2). |
| Sirota et al. (1995) | IL-2 | | colostrum | At concentrations as low as 0.5%, human colostrum stimulated IL-2 production; at a higher concentration (10%), IL-2 secretion was inhibited. |
| Melder and Jain (1992) | IL-2 | | | The increased rigidity of these cells was maintained throughout 96 h of IL-2 deprivation, although significant relaxation of rigidity was observed between 48 and 96 h. |
| Melder and Jain (1992) | IL-2 | | NK cells | Reintroduction of IL-2 for 24 h to a culture of NK cells depleted of IL-2 for 48 h did not restore the cells to the pre-depletion level of rigidity. |
| Melder and Jain (1992) | IL-2 | | NK cells | These findings suggest that the initial activation of human NK cells by IL-2 will produce a relatively rapid increase in rigidity that may cause entrapment of these cells in small capillaries in vivo and that removal of IL-2 will produce an additional increase in rigidity, which is associated with decreased functional activity.
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| Konrad et al. (1990) | IL-2 | | | The median serum IL-2 levels are 430-fold lower than levels in the i.p. fluid and decrease with a median half-life of 6.3 h.
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| Warrington (1988) | IL-2 | | | At high cell densities, IL-2 production was decreased in SLE but remained enhanced in RA. |
| Vetto et al. (1987) | interleukin-2 | | | Reduction of toxicity of interleukin-2 and lymphokine-activated killer cells in humans by the administration of corticosteroids.
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| Bygbjerg et al. (1987) | IL-2 | | lymphocytes | Pyrimethamine at concentrations above therapeutic levels suppressed the lymphocytes' proliferation, but not their IL-2 production. |
| Bygbjerg et al. (1987) | IL-2 | | lymphocyte | The IL-2 production was suppressed at concentrations twice as high as those required to suppress lymphocyte proliferation. |
| Reem et al. (1984) | IL-2 | | thymocyte | As a result of the inhibition of endogenous IL-2 synthesis, thymocyte proliferation at 120 h of culture was also inhibited. |
| Lomnitzer et al. (1984) | interleukin-2 | | | Suppression of interleukin-2 production by human concanavalin A-induced suppressor cells.
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| Lomnitzer et al. (1984) | IL-2 | | mononuclear cells | Con 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. |
| Lomnitzer et al. (1984) | IL-2 | | | These results show that Con A-treated MN cells suppressed or prevented [3H]thymidine incorporation by actively inhibiting IL-2 production.
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| Bonnard et al. (1979) | TCGF | | T cell | This loss of TCGF activity also occurred quite rapidly and was detectable within 1 hr of incubation of 0.3 ml supernatant with 2 to 5 x 10(7) CTC at 23 degrees C. 2 x 10(8) mononuclear peripheral blood leukocytes were not effective in removing TCGF activity, and incubation with similar numbers of cells from B and T cell lines had no effect. |
| McElhaney et al. (1990) | interleukin 2 | | | Age-related decline in interleukin 2 production in response to influenza vaccine.
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| McElhaney et al. (1990) | interleukin 2 | | helper T cells | Several studies have presented evidence to show that immune dysfunction in aged mice and humans may be due to a defect in the production of interleukin 2 (IL2) by helper T cells (TH). |
| McElhaney et al. (1990) | IL2 | | | This study provides evidence that defective IL2 production may also occur in response to physiologic antigenic stimulation and may be one explanation for the reduced efficacy of influenza vaccination in elderly persons.
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| Zaizov et al. (1986) | IL-2 | | leukocytes | Observed in all patients was impaired endogenous production of interleukin-2 (IL-2), expression of the IL-2 receptor combined with diminished responses to mitogens, mixed leukocytes reaction (MLR), and natural killer (NK) reactivity. |
| Wang et al. (1984) | IL-2 | | | Actinomycin D and puromycin inhibited the appearance of IL-2 receptors as well as the production of IL-2. |
| Marijani et al. (2007) | IL-2 | | | The bioactivity of ciclosporin MDI formulations was evaluated by determining the ciclosporin-mediated inhibition of interleukin-2 (IL-2) release from human Jurkat cells stimulated with phorbol 12-myristate 13-acetate (PMA). |
| Landsverk et al. (2002) | IL-2 gene | | T-cell | The normally repressed IL-2 gene is transcribed in nuclei from quiescent human T cells and from various non-T-cell lines. |
| Pahlavani and Richardson (1996) | IL-2 | | | The expression of IL-2 has been found to decrease with age in humans and rodents. |
| Pahlavani and Richardson (1996) | IL-2 | | | The decline in IL-2 production has been shown to parallel the age-related decrease in immunologic function. |
| Pahlavani and Richardson (1996) | IL-2 | | T cells | The age-related decline in IL-2 production has been shown to arise from a decline in IL-2 transcription, and a recent study suggests that the transcription factor NFAT (nuclear factor of activated T cells) may play a role in the decline in IL-2 transcription.
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| Prochazka et al. (1987) | IL-2 | | | These data collectively suggest that, in addition to impaired IL-2 production, there is an endogenous defect in IL-2 responsiveness. |
| Hoon et al. (1986) | IL-2 | | | When the IL-2 receptors were blocked with anti-Tac (anti-IL-2 receptor) antibodies, the inhibitory effect of IL-2 was significantly reduced. |
| Hoon et al. (1986) | IL-2 | | | Similarly antibody to IL-2 blocked the inhibitory effect of IL-2. |
| Honda and Steinberg (1984) | IL-2 | | PGE2 | The inhibitory effect of PGE2 on the responsiveness of T8+ cells was found to be due to inhibition of T4+-dependent IL-2 production. |
| Charley et al. (1985) | IL2 | | | Preculture of porcine PBL or addition of indomethacin enhanced IL2 production, suggesting the existence of a prostaglandin-mediated inhibition of IL2 production in fresh PBL cultures. |
| Arya et al. (1984) | cell growth factor | | T cell | Dexamethasone-mediated inhibition of human T cell growth factor and gamma-interferon messenger RNA.
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| Arya et al. (1984) | TCGF mRNA | | lymphocytes | Dexamethasone, a synthetic glucocorticoid, strongly inhibits the synthesis of TCGF mRNA in human normal peripheral blood lymphocytes stimulated in culture with phytohemagglutinin. |
| Toossi et al. (1986) | interleukin 2 | | | Defective interleukin 2 production and responsiveness in human pulmonary tuberculosis.
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| Domingo et al. (1985) | interleukin-2 | | lymphocyte | Human pregnancy serum inhibits proliferation of T8-depleted cells and their interleukin-2 synthesis in mixed lymphocyte cultures.
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| Domingo et al. (1985) | interleukin-2 | | T lymphocytes | T8-depleted and unfractionated T lymphocytes allogeneically stimulated and cultured in the presence of pregnancy sera exhibit an inhibition of cellular proliferation and interleukin-2 synthesis, respectively. |
| Domingo et al. (1985) | IL-2 | | lymphocyte | A possible mechanism to explain the inhibition of mixed lymphocyte cultures by pregnancy serum could therefore be decrease of cellular proliferation of the T8-depleted subpopulation with a decrease in IL-2 synthesis, implying an inhibition of cytotoxic effector cells.
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| Olejniczak and Kasprzak (2008) | IL-2 | | | Decreased IL-2 production is often observed in the more advanced clinical stages of human tumors, which provides rational for inclusion of recombinant IL-2 in the immunotherapy for some tumors. |
| Kenney et al. (1986) | IL-2 | | | Those test systems detect covalent and non-covalent aggregates, degradation products, and inappropriately oxidized forms of human interleukin-2 all of which contribute to an overall loss of IL-2 biological activity. |
| Sasagawa et al. (2006) | interleukin-2 | | T cells | Echinacea alkylamides inhibit interleukin-2 production by Jurkat T cells.
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| Sasagawa et al. (2006) | IL-2 | | | E. purpurea extracted in a solvent mixture of 95:5 ethanol/water dose-dependently inhibited IL-2 production. |
| Sasagawa et al. (2006) | IL-2 | | | Lower concentrations from 6.25 to 25 microg/mL significantly decreased IL-2 production but not cell viability. |
| Sasagawa et al. (2006) | IL-2 | | | Alkylamides at concentrations found in a 50 microg/mL extract decreased IL-2 production by approximately 50%. |
| Froelich et al. (1988) | interleukin-2 | | lymphocytes | Phytohemagglutinin induced proliferation by aged lymphocytes: reduced expression of high affinity interleukin-2 receptors and interleukin-2 secretion.
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| Pinkston et al. (1987) | interleukin 2 | | T lymphocytes | Corticosteroid therapy suppresses spontaneous interleukin 2 release and spontaneous proliferation of lung T lymphocytes of patients with active pulmonary sarcoidosis.
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| Pinkston et al. (1987) | IL 2 gene | | | In this regard, sarcoidosis represents a "model" human disorder to test in vivo the known in vitro action of corticosteroids on suppressing the activated IL 2 gene. |
| Pinkston et al. (1987) | IL 2 | | T cell | In contrast, over the same period, the treated group had marked reduction of spontaneous lung T cell release of IL 2 and proliferation (p less than 0.01, all comparisons before therapy). |
| Pinkston et al. (1987) | IL 2 gene | | T lymphocytes | These observations are consistent with the concept that directly, or indirectly, corticosteroids are capable of suppressing the IL 2 gene in activated T lymphocytes in vivo.
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| Ades et al. (1986) | IL-2 | | | Using human IL-2 or recombinant IL-2, we have found that monosaccharides inhibit IL-2 enhanced functional activity in a concentration-dependent fashion; that increased expression of endogenous monosaccharide binding receptors on effector cells occurs after treatment with IL-2; and that greater quantities of monosaccharide were required to obtain equivalent inhibition of IL-2 enhanced NK activity. |
| DeBruyne et al. (1995) | IL-2 | | | Therefore, nonresponsiveness to the allograft appeared to be due to a deficit in IL-2 production. |
| Kusugami et al. (1989) | interleukin 2 | | | However, cultures of Crohn's disease- and ulcerative colitis-derived cells contain significantly decreased interleukin 2 activity, suggesting that in vivo the availability of interleukin 2 may be limited, perhaps resulting in impaired cytotoxic function. |
| Kusugami et al. (1989) | interleukin 2 | | | In ulcerative colitis, a loss of interleukin 2-responsive cells, a hyporesponsiveness to interleukin 2, or both might be present. |
| Cadée et al. (2002) | rhIL-2 | | | The protein release profiles both the non-degradable and degradable dextran-based hydrogels showed that with increasing crosslink density of the gel, the release of rhIL-2 decreases. |
| Welte et al. (1984) | interleukin 2 | | bone marrow | Defective interleukin 2 production in patients after bone marrow transplantation and in vitro restoration of defective T lymphocyte proliferation by highly purified interleukin 2.
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| Welte et al. (1984) | IL2 | | PBMC | This 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. |
| Li and Weir (1990) | IL-2 | | | This inhibition is likely mediated through a reduction in both IL-2 production and IL-2 responsiveness. |
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