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

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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.
Pawelec et al. (1989)interleukin 2macrophagesTo study parameters of possible clonal anergy in such cells, lymphokine secretion before and after tolerisation was measured. 10/10 CD4+ clones were found to secrete interleukin 2 (IL-2), interferon gamma, tumour necrosis factor alpha and granulocyte/macrophages colony stimulating factors.
Smith (1992)interleukin-2macrophageChronic macrophage activation with subsequent failure of activated macrophages to properly control T-lymphocyte secretion of interleukin-2 and interleukin-2 receptors is proposed as the basic biological mechanism of schizophrenia.
Turgut et al. (2006)IL-2macrophagesThe aim of this study was to determine the effects of multidrug treatment on serum levels of interleukin-2 (IL-2), secreted by activated T cells, and of neopterin, secreted by macrophages and monocytes, in patients with pulmonary tuberculosis.
Lissoni et al. (1996)IL-2macrophageThis preliminary result, by showing an increased secretion of IL-12 in advanced cancer patients with IL-2 endogenous deficiency, would suggest the existance of a possible feedback mechanism operating between macrophage release of IL-12 and T lymphocyte secretion of IL-2.
Holch et al. (1989)IL2macrophageThere could be seen a decrease of parameters of cellular immunity (absolute lymphocyte count, CD-4-/CD-8-cell-ratio and release of IL2-receptors), a decrease of humoral defense (immunoglobulins and complement factors) and an increase of macrophage activation (serum levels of neopterin).
Smith and Maes (1995)interleukin-2macrophagesChronically activated macrophages and T-lymphocytes, along with excessive interleukin-2 and other cytokine secretions, were previously proposed as the fundamental mediators of schizophrenia.
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.
Leonard (2005)interleukin-2macrophagesThe T-helper 1 cells, that secrete interleukin-2 and interferon-gamma for example, are reduced in activity while the T-helper 2 cells, together with the macrophages, show an increased secretion of interleukins-6 and -10.
Deane et al. (2000)interleukin-2macrophageOrf virus encodes a novel secreted protein inhibitor of granulocyte-macrophage colony-stimulating factor and interleukin-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.
Migliaccio et al. (1997)IL-2macrophagesThe release of interleukin 2 (IL-2) and interferon gamma (IFN-gamma) by Th cells present in PBMC depleted of macrophages, or B cells is reported, after incubation in the presence of those peptides, fibronectin or Staphylococcus aureus protein A.
Marcinkiewicz et al. (1996)IL-2macrophagesBoth populations of macrophages after in vitro stimulation with IFN-gamma can inhibit IL-2 release.
Marcinkiewicz et al. (1996)IL-2macrophageFurthermore, NG-monomethyl-L-arginine monoacetate, a specific inhibitor of NO release had no effect on IL-2 release, while indomethacin, which blocked prostaglandin synthesis, largely abrogated the suppressor activity of both macrophage populations.
Marcinkiewicz et al. (1996)IL-2macrophageAlthough the addition of exogenous NO donors at high concentrations could inhibit IL-2 release by T cells, our data does not support the hypothesis that NO is a major macrophage mediator of suppression in this model.
Gavalas et al. (1998)IL-2macrophagesIn contrast, compound 2 significantly increased the IL-1 activity of arthritic macrophages while reducing the ability of normal and arthritic splenocytes to produce or release IL-2.
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.
Fonteneau et al. (1997)IL-2macrophageLysis 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.
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.
Matsubara et al. (1996)interleukin-2macrophageBoth cell lines were transduced retrovirally to secrete interleukin-2, interleukin-6 and granulocyte-macrophage colony-stimulating factor, respectively.
Goldyne and Stobo (1980)lymphokinemacrophagesProstaglandin (PG) E2, a major prostaglandin synthesized by human monocyte-macrophages is able to modulate a variety of T lymphocyte reactivities including blastogenesis, lymphokine secretion, and cytotoxicity.
Hancock et al. (1986)lymphokinemacrophageIn an investigation of the immunopathogenesis of sarcoidosis, the authors undertook the tissue localization of those lymphokines and lymphokine receptors which are known to play a central role in T-cell and macrophage activation.
Finocchiaro et al. (2008)interleukin-2macrophageWe evaluated the safety, efficacy and antitumor effects of direct intratumor injections of lipoplexes encoding herpes simplex thymidine kinase coadministrated with ganciclovir, and irradiated transgenic xenogeneic cells secreting 20-30 mug day(-1) of human granulocyte-macrophage colony-stimulating factor and interleukin-2.
Lissoni et al. (1992)IL-2macrophageOn the basis of the documented modulatory effect of IL-3 on macrophage functions, we have evaluated the influence of IL-3 on neopterin secretion during IL-2 immunotherapy.
Marselli et al. (2000)LymphokinemacrophageLymphokine release from human lymphomononuclear cells after co-culture with isolated pancreatic islets: effects of islet species, long-term culture, and monocyte-macrophage cell removal.
Buchmuller et al. (1985)lymphokinemacrophagesHuman blood mononuclear cells stimulated in vitro with concanavalin A secrete a lymphokine which activates mouse macrophages to kill Leishmania enriettii.
Demathé et al. (2008)IL-2macrophagesDevelopment of autoantibodies may be part of the nonspecific polyclonal B-cell stimulation seen in early stages of HIV infection secondary to interleukin (IL)-1 and IL-2 release by HIV-infected macrophages [9].
Zanin and Duvall (2009)IL-2macrophagesOnce the HIV viral load reaches zero, the HIT would be withdrawn and IL-2 or luteinizing hormone releasing hormone analogues (LHRH-A) might be administered to accelerate the natural replacement of the CD4(+) T(H) cells and macrophages.
Sheppard et al. (1983)lymphokinemacrophagesThe parent line and some clones passively transferred footpad DTH when injected locally, and some secreted a lymphokine activity that elicited intracellular killing of amastigotes within infected macrophages.
Murray (1988)lymphokinemacrophageRecent research on human macrophage activation has reemphasized the critical role of the lymphokine-secreting T cell in converting quiescent macrophages to efficient microbicidal phagocytes.
Murray (1988)lymphokinemacrophageInterferon-gamma, a key lymphokine secreted by antigen-triggered T4+ helper cells, is capable of inducing the macrophage to act against a diverse group of microbial targets, in particular, intracellular pathogens.
Lindén et al. (1999)interleukin-2macrophagesPACAP 1-38 enhances phagocytosis in macrophages and inhibits the release of the pro-inflammatory cytokine interleukin-2 in lymphocytes, suggesting antiinflammatory effects.
Geng and Hansson (1992)lymphokinemacrophagesWe have therefore studied the effect of interferon-gamma (IFN gamma), a lymphokine secreted by activated T lymphocytes, on the expression of ScR in human monocyte-derived macrophages.
van den Berg et al. (1980)lymphokinemacrophageSkin tests and macrophage migration inhibition measurements provided further support for the hypothesis that local lymphokine release may suppress the accumulation of eosinophils in chronic inflammatory lesions.
Marchand-Adam et al. (2005)IL-2macrophagesT lymphocytes proliferate in response to beryllium antigens and combined with macrophages produce numerous epithelioid granulomas with the release of inflammatory cytokines (IFNgamma, IL-2, TNFalpha and IL6) and growth factors.
Fang et al. (2008)IL-2macrophagesBoth IL-2, a secreted cytokine important for the proliferation of T and B lymphocytes, and TNF, a multifunctional proinflammatory cytokine secreted by macrophages, are also known to be involved in cytokine-cytokine receptor interaction, which can be found from our database gene search.
Nelson et al. (1994)Interleukin-2macrophagesInterleukin-2 suppresses activated macrophage intracellular killing activity by inducing macrophages to secrete TGF-beta.
Lobo and Patel (1997)IL-2macrophagesOf interest, OKT3D(IgG1) in its intact form, but not its F(ab')2, activated HuT-78 to secrete IL-2 in the absence of U937 suggesting therefore that OKT3D activates T cells in the absence of macrophages and provided its Fc domain is intact.
Selvey et al. (2004)IL-2macrophagesIL-2 is also released by tumour infiltrating lymphocytes (TILs) and IL-6 is released by tumour associated macrophages (TAMs), TILs and fibroblasts [16,20-22].
Ouyang et al. (2006)IL-2TAMIn addition, TAM recovered from B16/IL-2 secreted 33.64 times more IFNgamma in response to in vitro administration of IL-2.
Cruz Cubas et al. (1993)IL-2macrophagesIL-2, IL-4, IL-5, IFN-gamma cytokines secreted principally by CD4+ T lymphocytes and oxygen and nitrogen radicals produced by activated macrophages, are involved in the control of plasmodial infection.
Pohla et al. (1993)IL-2macrophageAfter stimulation, the cells secreted tumor necrosis factor alpha and granulocyte/macrophage colony-stimulating factor (GM-CSF) detected by immunoassays, and T-cell growth factors, most likely IL-2, as detected by bioassays.
Agrewala et al. (1998)interleukin-2macrophagesIn the present study, we provide evidence that in a T-dependent antigen-driven system, the signals generated by hapten-specific B cells to stimulate Th cells for the secretion of interleukin-2 (IL-2), interferon-gamma (IFN-gamma), and IL-4 were differentially modified by M150, a 150-kDa molecule expressed on the surface of macrophages.
Homolka et al. (2003)IL-2macrophageWe chose tumor necrosis factor-alpha (TNFalpha) since it is a cytokine predominantly secreted by cells of the monocyte/macrophage lineage and interleukin-2 (IL-2) exclusively by T lymphocytes.
MacSween et al. (1982)lymphokinemacrophageWhile the phenomenon of macrophage migration inhibition is a useful indicator of lymphokine release, it may be caused by other substances, it is subject to considerable variability, and it may be masked by the concomitant presence of substances stimulating migration.
Mikuni (1995)IL-2MacrophagesInterleukin-2 (IL-2), mainly secreted by activated T-cells, influences other T-cells, B-cells, Macrophages, NKcells, etc. and is a major proliferating and differentiation factor of lymphocytes.
Ogawa et al. (2008)IL-2macrophagesOriginally named "cytokine synthesis inhibitory factor" for its ability to inhibit IFN-gamma and IL-2 production in Th2 cells, it is secreted by monocytes, macrophages, mast cells, T and B lymphocytes, and dendritic cells (DCs).
Bruserud (1998)IL-2macrophageA majority of both CD4+ and CD8+ clones secreted detectable interleukin-2 (IL-2), IL-10, IL-13, granulocyte/macrophage-colony-stimulating factor and interferon gamma (IFNgamma) in response to phytohaemagglutinin + accessory cells (Epstein-Barr-virus-transformed B cell line, 80-Gy-irradiated).
Kovacs and Kelley (1985)lymphokinemacrophagesTo test whether lymphokine(s) secreted by alveolar lymphocytes regulated MDGF secretion by macrophages in this model, the authors exposed normal macrophages harvested from control rat lungs to lymphokine preparations in vitro.
Liu et al. (2009)IL-2macrophageThen the supernatant were collected to detect the levels of granulocyte/macrophage colony stimulating factor (GM-CSF), interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1 beta), IL-2, IL-4, IL-6, IL-8, IL-10, and IL-12 by using LiquiChip system.
Álvaro et al. (2010)IL-2macrophagesAmong natural cytotoxic cells, natural killer cells (NK cells) can be activated directly by contact with the tumor or as a result of the stimulus provided by cytokines such as interferons, TNF, IL-2, and IL-12, released by tumor-specific T lymphocytes and macrophages; therefore, their activity is endowed with some degree of specificity.
Leong et al. (2002)interleukin-2macrophageMETHODS: A portion of each SLN from 68 melanoma patients undergoing selective SLN dissection was processed for enzyme-linked immunospot (ELISPOT) assay determination of interferon gamma (IFN-gamma), interleukin-2 (IL-2), granulocyte macrophage colony-stimulating factor (GM-CSF), and interleukin-10 (IL-10) secretion.
Panayi (1999)IL-2macrophagesFollowing activation, T cells initiate the inflammatory cascade through secretion of either interleukin 2 (IL-2) or interferon gamma, or through direct cellular interaction with macrophages and synoviocytes.
Lamperi and Carozzi (1988)lymphokinemacrophagesIn some CAPD patients a disturbance in lymphokine and monokine release may be responsible for the reduced ability of their macrophages to kill bacteria.
Kast (1980)lymphokinemacrophageAggregation results in lymphokine release that makes the macrophage electrophoretic mobility test and variants positive.
Ramachandra and Wikel (1992)interleukin-2macrophagesCytokines assessed in this study included interleukin-1, IL-1, and tumor necrosis factor (TNF) alpha produced by macrophages, and interleukin-2, IL-2, and gamma interferon (IFN-G) secreted by T-lymphocytes.
Schultz (1987)interleukin-2macrophagesUpon activation, macrophages release interleukin-1 (alias lymphocyte activating factor, leukocytic endogenous mediator, and endogenous pyrogen), a family of molecules with multivarious biological effects, ranging from induction of fever and the acute phase response to lymphocyte activation and concomitant release of interleukin-2.
Weaver et al. (1989)lymphokinemacrophageBoth types of clones also induced macrophage mIL-1 by cell-cell contact (i.e., in the absence of lymphokine release).
Gorter et al. (2003)IL-2macrophageThe release of interleukin (IL)-1alpha, IL-2, IL-6, IL-8, IL-10, IL-12p(40+70), IL-12p(70), tumor necrosis factor-alpha (TNFalpha), interferon (IFN)-alpha, IFNgamma, granulocyte macrophage-colony stimulating factor, and RANTES was determined after incubation with 0.5 ng/mL of IQuS ng/mL and VaQuFrF.
Ouyang et al. (2006)IL-2TAMTAM expressed both asialo GM1 and CD11b antigen, and TAM recovered from B16/IL-2 produced interferon gamma (IFNgamma) 6 times more than that from B16/mock.
Choi et al. (1990)Interleukin-2macrophageDuring the activation of T-cell by Interleukin-1 released from the macrophage, not only Interleukin-2 but also the soluble Interleukin-2 receptor (sIL-2R) molecule is released into the extracellular fluid.
Rogy et al. (2000)interleukin 2macrophagesThe release of interleukin 2 (IL-2) and Interferon-gamma (IFN-gamma) by naive T lymphocytes predominantly stimulates cytotoxic T lymphocytes, macrophages, and natural killer (NK) cells and increases the antigen-presenting potential of all these cell types.
Honda et al. (1985)lymphokinemacrophageMCF-c shared common antigenicity with the macrophage chemotactic lymphokine released from bovine gamma globulin (BGG) and horse radish peroxidase (HRPO) -stimulated lymphocytes, using an immunoadsorbent column conjugated with anti-MCF-c antibody.
Kurnatowski and Kurnatowska (2010)IL-2macrophagesTh2 lymphocytes, on the other hand, suppress cellular immunity by releasing the cytokines IL-4, IL-6 and IL-10 which counter regulate the secretion of IL-2, IL-12, IFN gamma and depress the activity of macrophages.
Hatzelmann and Schudt (2001)IL-2macrophagesThe anti-inflammatory and immunomodulatory potential of roflumilast and the reference compounds was investigated in various human leukocytes using cell-specific responses: neutrophils [N-formyl-methyl-leucyl-phenylalanine (fMLP)-induced formation of LTB(4) and reactive oxygen species (ROS)], eosinophils (fMLP- and C5a-induced ROS formation), monocytes, monocyte-derived macrophages, and dendritic cells (lipopolysaccharide-induced tumor necrosis factor-alpha synthesis), and CD4+ T cells (anti-CD3/anti-CD28 monoclonal antibody-stimulated proliferation, IL-2, IL-4, IL-5, and interferon-gamma release).
Butt et al. (2009)interleukin-2macrophageGarlic could be useful in preventing the suppression of immune response associated with increased risk of malignancy as it stimulates the proliferation of lymphocytes, macrophage phagocytosis, stimulates the release of interleukin-2, tumor necrosis factor-alpha and interferon-gamma, and enhances natural killer cells.
Barnes et al. (1992)IL-2macrophageMeasurement of concentrations of TNF, granulocyte-macrophage-CSF, IL-6, IL-10, IFN-gamma, IL-2, and IL-4 in cell culture supernatants indicated that cytokine release correlated with mRNA patterns.
Gauduin et al. (1999)IL-2macrophageSIV-specific stimulation of lymphocytes from vaccinated macaques resulted in secretion of interferon-gamma, IL-2, regulated-upon-activation, normal T cells expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1alpha, and MIP-1beta but not IL-4 or IL-10.
van Seventer et al. (1991)IL-2macrophageThe integrins also regulate the secretion of IL-2, IL-4, and granulocyte/macrophage colony-stimulating factor.
Yung et al. (1995)IL-2macrophagesTreated, but not untreated, cells responded to syngeneic APCs without Ag, overexpressed LFA-1, spontaneously lysed syngeneic macrophages, and secreted relatively large amounts of IL-6, small amounts of IL-4, and no detectable IL-2 nor IFN-gamma.
Sim et al. (1994)IL-2macrophageTo study the role of cytokines in allergic late-phase reactions (LPR), we measured cytokines (interleukins [IL]-1 beta, IL-2, IL-4, IL-5, IL-6, and granulocyte-macrophage colony-stimulating factor [GM-CSF]) in nasal secretions (NS) of eight allergic subjects following antigen or saline provocation.
Sharma et al. (2007)lymphokinemacrophagesThe most striking findings were that both resveratrol and curcumin suppressed the activity of T and B cells and macrophages, as evidenced by significant inhibition in proliferation, antibody production and lymphokine secretion.
Baker et al. (1993)IL-2macrophageOn stimulation these four clones secreted high levels of gamma-interferon and detectable levels of IL-2, IL-10 and granulocyte/macrophage colony stimulating factor (GM-CSF) depending upon the nature of the stimulus, but no IL-4 or TNF-alpha production was detected.
Lamm and Riggs (2001)interleukin-2macrophagesBoth stimulate proliferation of lymphocytes and macrophage phagocytosis, induce the infiltration of macrophages and lymphocytes in transplanted tumors, induce splenic hypertrophy, stimulate release of interleukin-2, tumor necrosis factor-alpha and interferon-gamma, enhance natural killer cell, killer cell and lymphokine-activated killer cell activity.
Thunell et al. (2010)IL-2macrophageFollowing initial therapy, 13 of the 16 detectable cytokines and chemokines decreased significantly in diseased sites, including IL-1alpha, IL-1beta, IL-2, IL-3, IL-6, IL-7, IL-8, IL-12 (p40), CCL5/regulated on activation, normally T cell expressed and secreted (RANTES), eotaxin, macrophage chemotactic protein-1, macrophage inflammatory protein-1alpha and interferon-gamma.
Atkins and Francis (1985)lymphokinemacrophagesMonocytes or macrophages may be induced to produce IL 1 by activators (e.g., lipopolysaccharide endotoxin) that act directly or by antigens/mitogens (e.g., Con A) that stimulate inducer lymphocytes to release a lymphokine that stimulates macrophages.
Bleijs et al. (1999)IL-2macrophageGranulocyte-macrophage colony-stimulating factor and IFN-gamma were secreted in high amounts, whereas IL-2, IL-4 and IL-5 could not be detected.
Arai et al. (1990)IL-2macrophagesIn response to antigenic stimulation, T cells and macrophages secrete a set of glycoproteins termed lymphokines and monokines such as IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, GM-CSF, G-CSF, IFN-alpha, IFN-gamma, TNF-alpha, and lymphotoxin.
Oddera et al. (1995)IL-2macrophageAllergen-induced T-cell proliferation was associated with increased HLA-DR antigen and IL-2 receptor expression (P < 0.001), and with increased release of IL-2, interferon-gamma (IFN-gamma), IL-1 beta, tumor necrosis factor-alpha (TNF-alpha), and granulocyte/macrophage colony-stimulating factor (GM-CSF).