Viewing affirmative mentions of positive regulation of IL2 (H. sapiens) in macrophages

Full-text article links are indicated by after the article reference.

Document Target Regulator Anatomy Sentence
Solbach et al. (1982)Il-2macrophageMacrophages are also required for Il-2 production, but the macrophage requirement can be bypassed by a soluble macrophage product as found in supernatants of lymphocyte cultures stimulated with lipopolysaccharide (LPS), the biological activity presumably representing Interleukin-1 (Il-1).
Paetkau et al. (1980)IL2macrophagesFinally, IL2 does not adequately restore a secondary response to the purified protein derivative of tuberculin (PPD) in adherent-cell-depleted cultures, indicating that macrophages, in addition to being required for IL2 production, have other functions.
Lipkowitz et al. (1984)IL 2macrophagesThe production of IL 2 by T lymphocytes cultured with NAGO-treated macrophages closely paralleled the induction of IL 2 receptors on the T lymphocytes.
Lissoni et al. (1993)interleukin-2macrophageThe concomitant generation of macrophage-mediated suppressive events, as documented by the increase in neopterin and soluble interleukin-2 (IL-2) receptor (SIL-2R), and the enhanced production of cortisol, would represent the most investigated phenomena responsible for the reduced anticancer efficacy of IL-2 immunotherapy in humans.
Shaw et al. (1987)Interleukin-2macrophagesThe induction of Interleukin-2, Interferon gamma and the Colony Stimulating Factor for granulocytes and macrophages was suppressed by Cyclosporin A at moderate concns.
Tatsumi and Yabe (1986)IL 2macrophagesAdherent macrophages appeared to inhibit rather than enhance IL 2 production in this system.
Shirakawa et al. (1986)interleukin 2macrophagesThe role of macrophages (monocytes) for the induction of interleukin 2 receptors (IL 2R) on human B lymphocytes was studied by a direct immunofluorescence method with the use of a fluoresceinated anti-IL 2R monoclonal antibody and a flow cytofluorometer.
Larsson and Coutinho (1984)IL 2macrophagesI-A antigens appear, therefore, to play two distinct roles in the induction of IL 2 production: (a) I-A molecules are directly involved in mediating activation signals to the macrophages at the level of IL 1 production; (b) I-A epitopes act as restricting elements in specific antigen recognition by T helper cells at the level of IL 2 production, a requirement which is overcome by lectin.
Kaczmarek et al. (1985)IL-2macrophageOnly two (2F1 and the IL-2 receptor) are increased in PHA-stimulated macrophage depleted cultures.
Böni-Schnetzler et al. (1985)TCGFmacrophagesThis is further supported by the failure to reconstitute the suppressed mitogenic response with normal macrophages, which are involved in activation of TCGF producer T-cells.
Cheng et al. (1996)IL-2macrophageProstate-specific antigen (PSA) levels in the cell culture media were monitored after transfecting CWR22 cells with candidate therapeutic genes, including the cytokines human interleukin 2 (IL-2) and granulocyte-macrophage colony-stimulating factor (GM-CSF), both as complementary DNAs [cDNAs]).
Yanagawa et al. (1989)IL-2macrophagesDaily injections of IL-2 resulted in reduction in the up-regulation of LAK induction by pleural macrophages and also in increases in the levels of soluble IL-2 receptors in pleural effusions.
Okada et al. (1981)IL-2macrophagesIn a clone (38-B) that did not show any IL-2 activity in culture supernatants, the addition of macrophages induced IL-2 production in the presence of phytohemagglutinin, suggesting that interleukin-1 induced IL-2 production in T hybrid cells.
Nagashima et al. (1997)IL-2-secretingmacrophagesTumor regression was mediated by numerous mononuclear cells, identified as murine NK cells and macrophages by immunohistochemistry, which accumulated around the IL-2-secreting, but not parental, tumors within 5-6 days after tumor cell injections.
Lipkowitz et al. (1984)IL 2macrophagesDespite early expression of receptors for IL 2 and early production of IL 2 by T lymphocytes during activation, T lymphocytes were not committed to proliferate in the absence of IL 2 until more than 24 hr of incubation with NAGO-treated macrophages had elapsed.
Nakamura et al. (1991)IL-2macrophagesThe expression of p75 IL-2 receptor on CD4+ T cells was induced by coculture with macrophages.
Nakamura et al. (1991)IL-2macrophageThe macrophage-induced p75 IL-2 receptor acquisition was blocked by monoclonal antibody (mAb) against class II antigen.
Benson and Ziegler (1989)IL-2macrophageIn order to understand the mechanism of immunosuppression by cyclosporine, its effects on macrophage-mediated antigen-specific T cell activation (IL-2 production) were studied in vitro.
Itescu et al. (1996)IL-2macrophageThese results demonstrate that humans contain circulating NK cells capable of lysing PAEC after activation with IL-2, that the mechanism involves interactions between CD2 and its ligand on porcine endothelium, and that these interactions may be influenced by macrophage-derived cytokines produced at the site of xenograft rejection.
Abramson et al. (1983)interleukin 2macrophagesTo investigate mechanisms by which antigen, macrophages, and interleukin 2 (IL2) participate in the induction of secondary T-cell proliferative responses, trinitrophenyl (TNP) was presented in three distinct modes: (i) TNP-modified peripheral blood mononuclear cells (TNP-PBMC), (ii) TNP-PBMC cell sonicates, and (iii) TNP-ovalbumin (TNP-OVA).
Abramson et al. (1983)interleukin 2macrophagesRequirements for Mac-120+ macrophages and responsiveness to interleukin 2.
Shirakawa et al. (1986)interleukin 2macrophagesRequirement of macrophages (monocytes) for the induction of interleukin 2 receptors on B lymphocytes.
Cox et al. (2008)interleukin-2macrophageThe samples were tested using a statistically qualified nine-color intracellular cytokine staining assay measuring interleukin-2 (IL-2), tumor necrosis factor alpha, macrophage inflammatory protein 1beta, and gamma interferon production and expression of CD107a.
Skansén-Saphir et al. (1994)IL-2macrophageCells were harvested after 48 or 72 h of culture and stained for the following cytokines: interleukin(IL)-1 alpha, IL-1 beta, IL-1ra, IL-6, IL-8, IL-2, tumor necrosis factor interferon(IFN)-gamma and TNF-alpha and TNF-beta and granulocyte macrophage-colony-stimulating factor.
Caspritz and Hadden (1987)interleukin 2macrophageThe usefulness of thymic hormones, interleukin 2, macrophage growth factor/colony stimulating factor, and interferons as immunotherapeutic agents is considered.
Uchiyama et al. (1987)IL-2macrophagesReconstituted cell cultures of nylon wool column-passed T cells and macrophages produced IL-2 by TSST-1 stimulation and, furthermore, the accessory activity of the macrophages could be partially replaced by a macrophage-derived factor containing interleukin 1.
Foon et al. (1985)interleukin-2macrophageSupernatants of these cultures were screened for interleukin-2 (IL-2), chemotactic factor, interferon, migration inhibition factor, and macrophage-activating factor activities.
Yarbrough et al. (1994)interleukin-2macrophagesInhibition of lymphokine-activated killer cells by human pulmonary macrophages: discordance between up-regulation of the beta chain (p75) of the interleukin-2 receptor on CD56+ cells and limited response to interleukin-2.
Girard et al. (1995)IL-2macrophageHowever, when cells were stimulated with the combination of a fixed concentration of granulocyte-macrophage colony-stimulating factor (GM-CSF), a dose-dependent effect of IL-2 was observed on the induction of both RNA and protein synthesis.
Burkitt and Aggarwal (2000)IL-2macrophagesAfter "poly-plat" treatment macrophages developed cytoplasmic extensions much faster and secreted higher levels of interleukin-2 (IL-2), compared to CDDP.
Han et al. (1999)IL-2macrophageRESULTS: IL-2 enhances the cytotoxicity of the standard IFNgamma/LPS macrophage activation in this system.
Fülöp et al. (1997)IL-2macrophageThe stimulating agents included: phorbol myristate acetate (PMA), hydrogen peroxide (H2O2), N-formyl-methionyl-leucyl phenylalanine (FMLP), granulocyte-macrophage colony stimulating factor (GM-CSF), reduced glutathione (GSH), lipopolysaccharide (LPS) and interleukin 2 (IL-2).
Murray et al. (1985)IL-2macrophageTo test the hypothesis that deficient interleukin 2 (IL-2) secretion may underlie the impaired capacity of T cells from patients with Acquired Immunodeficiency Syndrome (AIDS) and the AIDS-related complex (ARC) to generate the macrophage-activating lymphokine, gamma interferon (IFN-gamma), we used five specific microbial antigens to examine IL-2 production.
Brach et al. (1993)IL-2macrophageHere we report that binding of human IL-2 to its binding site leads to transcriptional activation of the macrophage CSF (M-CSF) gene in Mo resulting in accumulation of M-CSF mRNA and subsequent release of bioactive M-CSF protein as demonstrated by ELISA and inhibition of IL-2 induced release of an activity-stimulating growth of monocyte-type colonies by a neutralizing anti-M-CSF antibody.
Bacchetta et al. (1990)IL-2macrophageFurthermore, different modes of activation resulted in simultaneous production of IL-5, IL-2, IFN-gamma, granulocyte/macrophage-CSF, and transcription of the TNF-beta gene by the host-reactive clones, indicating that the lack of IL-4 production is not related to the mode of activation.
Singh et al. (1989)IL-2macrophageUp-regulation by granulocyte-macrophage colony-stimulating factor (GM-CSF) of induction of lymphokine (IL-2)-activated killer (LAK) cells by human blood monocytes.
Chujor et al. (1992)IL-2macrophageInterestingly, LAM exhibited a down-regulatory effect on the accumulation of mRNAs for IL-2, IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-2 receptor alpha (IL-2R alpha) in T cells co-stimulated with phytohaemagglutinin-P (PHA) and 4 beta-phorbol-12-myristyl-13-acetate (PMA).
Sztein and Serrate (1989)IL-2macrophagesHowever, macrophages are an absolute requirement during the exposure to the mitogen after preincubation with thymosins for the manifestation of TF5- and T alpha 1-mediated enhancing effects on IL-2 production and IL-2R expression.
Andreesen et al. (1983)lymphokinemacrophageEnhancement of spontaneous and lymphokine activated human macrophage cytotoxicity by hyperthermia.
Andreesen et al. (1983)lymphokinemacrophagesIn addition, lymphokine activation of macrophages for cytotoxicity appeared to be more effective at elevated temperatures.
Sypek and Wyler (1988)lymphokinemacrophageIn the present study we determined that strains of Leishmania mexicana that are not susceptible to the antimicrobial effects that result from lymphokine activation are nonetheless susceptible to antileishmanial effects resulting from T cell contact-mediated macrophage activation.
Gilbreath et al. (1985)lymphokineMacrophageMacrophage activation for microbicidal activity against Leishmania major: inhibition of lymphokine activation by phosphatidylcholine-phosphatidylserine liposomes.
Masur et al. (1982)lymphokinemacrophagesThe presence of pharmacological concentrations of HC before or during lymphokine activation prevented normal macrophages from acquiring the capacity to either respond oxidatively to Toxoplasma gondii ingestion or to inhibit intracellular toxoplasma replication.
Lundy and Lovett (1978)lymphokinemacrophageOne cell population potentiated by TBZ is the macrophage, either by direct activation or secondary to increased lymphokine production.
Farrar et al. (1981)IL 2macrophageThese findings are consistent with the hypothesis that the induction of CTL involves a linear cell-factor interaction in which IL 1 (macrophage-derived) stimulates T cells to produce IL 2, which in turn stimulates other T cells to produce immune interferon and become cytotoxic.
Fonteneau et al. (1997)IL-2macrophageAs a consequence, most melanoma lines, including those with the highest Ag expression, could trigger only low CTL fractions to secrete IL-2 and, also for most clones, granulocyte-macrophage CSF.
Roussel et al. (1995)LymphokinemacrophageLymphokine gene activation in TIL was assessed by mRNA reverse transcriptase/polymerase chain reaction (RT-PCR) and primers for interleukin(IL)-2, IL-4, interferon (IFN) gamma, granulocyte/macrophage-colony-stimulating factor (GM-CSF), and tumor necrosis factor (TNF) beta.
Carel et al. (1983)interleukin 2macrophagesFurthermore, supernatants derived from syngeneic macrophages pulsed with the relevant peptide also induced the antigen-specific hybridoma to produce interleukin 2.
Peters et al. (1985)lymphokinemacrophageIn particular, with the availability of recombinant gamma interferon (rIFN-gamma) a variety of immuno-regulatory functions, including natural killer activation, enhancement of lymphokine production, macrophage activation, and cell surface Ia expression, have been clearly shown to be mediated by this lymphokine.
Tilg et al. (1995)IL-2macrophagesPeripheral blood mononuclear cells and in vitro-derived macrophages synthesized similar amounts of IL-10 after stimulation with IL-1 alpha or IL-2, but were unresponsive to IL-6.
Ehlers and Smith (1991)IL-2macrophageComparison of neonatal and adult T cells revealed that both populations expressed the genes for interleukin 2 (IL-2) and its receptor, but only adult T cells were capable of transcribing mRNAs for IL-3, IL-4, IL-5, IL-6, interferon gamma, and granulocyte/macrophage colony-stimulating factor.
von Wussow et al. (1990)IL2macrophageNeither interleukin (IL) 1 nor IL3, IL4, IL5, IL6, tumor necrosis factor-alpha/beta, granulocyte colony-stimulating factor (CSF) or granulocyte macrophage-CSF at any of the concentrations tested were capable of eliciting any detectable amount of the Mx homolog, while IL2 was a poor Mx-homologous protein inducer.
Fonteneau et al. (1997)lymphokinemacrophageLysis and secretion of IFN-gamma, and for most clones' secretion of TNF-alpha, required lower Ag densities, by one or two logs, than IL-2 and granulocyte-macrophage CSF secretion. 3) In a significant fraction of IFN-gamma-secreting cells, IL-2 production is not induced. 4) A large fraction of cloned cells is refractory to lymphokine gene activation for about 2 wk after previous stimulation.
Loo et al. (2010)IL-2macrophageThe levels of IL-2, IL-4, granulocyte-macrophage colony-stimulating factor and the mRNA content of these cytokines were also enhanced.
Makhoul et al. (1987)interleukin-2macrophageMitogenic doses of membranes purified from Mycoplasma pneumoniae as well as concanavalin A (ConA) were tested for their ability to induce production of interleukin-2 (IL-2) and granulocyte-macrophage colony-stimulating activity (GM-CSA) by human peripheral blood mononuclear cells.
Ellis et al. (1991)IL2macrophagesThe results were similar in the tertiary alloresponse except that (a) IL4 was now detectable in the supernatants but only where dendritic cells had been used as APC, and (b) both resting and activated macrophages induced IL2 and IFN-gamma.
Fujiwara and Ellner (1986)IL 2macrophageThe human macrophage-like cell line U937 spontaneously produced a nondialyzable factor that inhibited interleukin 1 (IL 1), interleukin 2 (IL 2), and phytohemagglutinin (PHA)-induced blastogenesis in mouse thymocytes.
Chung et al. (1991)IL-2macrophagesIn contrast, dmPGE2 (10(-12)-10(-6) M) inhibited both the induction of MPIF and the ability of MPIF directly to induce macrophages to express PCA, with lesser effects on the induction of IL-2.
de Moerloose et al. (1986)lymphokinemacrophagePertussigen thus induces an increase in lymphokine(s) production responsible for the in vitro increase in macrophage mPCA and PA activity and which may be responsible for some of the potent immune effects of this agent in vivo.
Fortin et al. (1997)IL-2macrophageRESULTS: Addition of BF d-12 in the culture medium induced a strong inhibition of IL-2, TNF-alpha, IL-10, and granulocyte-macrophage colony-stimulating factor (GM-CSF) production.
Chen et al. (2005)interleukin-2macrophageUsing chromatin immunoprecipitation, we observed an apparent decrease of histone acetylation and phosphorylation signals at the proximal promoter region of the inducible interleukin-2 and granulocyte-macrophage colony-stimulating factor genes in response to T-cell activation.
Tovar et al. (1988)IL-2macrophageThis synergistic response is macrophage independent, greatest at low concentrations of anti-CD3, inhibited by anti-IL2 receptor, and depends upon the induction of IL-2 receptors by CD3 activation which are then available to respond to exogenously added IL-2.
Ausiello et al. (1993)IL-2macrophageMP, PPD, and IL-2 induced appreciable levels of granulocyte-macrophage colony-stimulating factor and gamma interferon, but only MP and PPD were able to induce IL-2 mRNA.
van Bezooijen et al. (1996)IL-2macrophageThe present data suggest that more of the patients with no or moderate HLA-II expression and/or no or moderate macrophage presence in the primary tumor could survive with persistence of their malignant disease after having received IL-2 immunotherapy, as compared to patients with both high HLA-II and high macrophage expression.
Vitolo et al. (1994)IL-2macrophagesMessenger RNA expression for interleukins (IL) IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-10, tumor necrosis factor-alpha, transforming growth factor-beta, interferon-gamma, granulocyte-macrophages colony stimulating factor, and human perforin-1 was assessed by in situ hybridization on the same tissues.
Bendtzen and Petersen (1984)lymphokinemacrophagesRole of monocytes/macrophages and interleukin 1 in antigen-induced human lymphokine production.
Bendtzen and Petersen (1984)lymphokinemacrophageThe monocyte/macrophage (M phi)-dependency for antigen-induced production of the lymphokine, leukocyte migration inhibitory factor (LIF), was investigated using a M phi pulse-exposure technique.
Hojo and Hiramine (1979)lymphokineMphiAn attempt has been made to characterize the cell type which releases blastogenic factor(s) (BF) on purified protein derivative (PPD) stimulation in complete Freund's adjuvant (CFA)-sensitized guinea-pig system and, further, to examine whether macrophages (Mphi) are required for antigen activation of T or B lymphocytes to produce this lymphokine.
Girard and Fernandes (1977)lymphokinemacrophagesThe stimulation of lymphokine producing T cells also need the presence of healthy macrophages.
Smith et al. (1998)IL-2TBMFurthermore, addition of TBM to IL- 2-inducing positive controls (B cells) not only failed to augment IL-2 production, but rather TBM significantly (55-90%) reduced B-cell induction of IL-2.
Chung et al. (1991)interleukin-2macrophageSince our previous studies have suggested that macrophage procoagulant activity (PCA) is an important mediator of allograft rejection, in this study we have examined the effects of CsA and 16,16 dimethyl prostaglandin E2 (dmPGE2) alone and in combination on the induction of macrophage PCA and on the lymphokines macrophage procoagulant-inducing factor (MPIF) and interleukin-2 (IL-2) in vitro.
Irving et al. (1990)lymphokinemacrophageThe genomic organization of two newly described induced lymphokine genes, 464.1 and 744.1, has been determined. 464.1 and 744.1 appear to be the human homologues of the recently cloned murine macrophage inflammatory proteins, MIP-1 alpha and MIP-1 beta, respectively.
Lu et al. (2007)IL-2macrophageTHP-1 macrophage-like cells exposed with PLGA-rAg85B microspheres induced the DB-1 cells to produce IL-2 at a level that was two orders of magnitude larger than the response elicited by soluble rAg85B.
Lissoni et al. (1993)IL-2macrophageIn previous studies, the authors observed that the increase in the soluble IL-2 receptor (SIL-2R) and neopterin levels was related to the generation of macrophage-mediated immunosuppression and associated with a reduced clinical efficacy during IL-2 cancer immunotherapy.
Koka et al. (2003)IL-2macrophageThe levels of interleukin 6 (IL-6), interferon gamma (IFN-gamma), and IL-2 RNAs increased and macrophage inflammatory protein 1beta (MIP-1beta) RNA decreased significantly in infected thymocytes.
Feske et al. (2000)IL-2macrophageThis transient activation of NFAT was not sufficient to induce the expression of several cytokines, including IL-2, IL-3, IL-4, and IFN-gamma, whereas mRNA levels for macrophage inflammatory protein-1alpha, GM-CSF, and IL-13 were only moderately reduced.
Pati et al. (2003)IL-2macrophageNF-AT activation by vGPCR depended upon signaling through the phosphatidylinositol 3-kinase-Akt-glycogen synthetase kinase 3 (PI3-K/Akt/GSK-3) pathway and resulted in increased expression of NF-AT-dependent cell surface molecules (CD25, CD29, Fas ligand), proinflammatory cytokines (interleukin-2 [IL-2], IL-4), and proangiogenic factors (granulocyte-macrophage colony-stimulating factor GMCSF and TNF alpha). vGPCR expression also increased endothelial cell-T-cell adhesion.