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

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Watson et al. (1991)IL-2NK cellsThe increase in the percentage of cells with markers of NK cells and in expression of IL-2 receptors was dose dependent.
Toossi et al. (1989)interleukin 2large granular lymphocytesPeripheral blood large granular lymphocytes (LGL) expressing Leu 11 (CD16) antigen with potent natural killer cytotoxicity inhibited soluble antigen-induced T-cell production of interleukin 2 (IL-2).
Tartour et al. (2000)IL-2natural killer cellThe relationship between local treatment and tumour regression was supported by replacement of tumour cells by inflammatory cells in regressing lesions and marked induction of T and natural killer cell derived cytokines (IL-2, IL-4, IFNg ...) in post-therapeutic lesions analysed 28 days after the start of Vero-IL-2 administration.
Waldmann and Tsudo (1988)IL-2large granular lymphocytesThe p75 peptide is the receptor for IL-2 on large granular lymphocytes and is sufficient for the IL-2 activation of these cells.
Vujanovic et al. (1993)IL2NK cellsIn the presence of 22 nM of interleukin 2(IL2), a substantial proportion of resting (R)-NK cells developed adherence to plastic as early as after 5 min of IL2 incubation, and by 1-5 hr of IL2 induction, 16% (range, 4-30%) of NK cells were adherent.
Aoki and Fukuchi (1987)interleukin-2natural killer cellMedullasin enhances human natural killer cell activity by a mechanism other than the induction of interferons or interleukin-2.
Aoki and Fukuchi (1987)interleukin-2natural killer cellThese results indicate that the mechanism of activation of human natural killer cell activity by medullasin is not mediated by the induction of interferons or interleukin-2.
Goldfarb et al. (1998)IL-2natural killer cellAugmentation of IL-2 activated natural killer cell adoptive immunotherapy with cyclophosphamide.
Galli et al. (1990)IL-2LGLIn addition, MAb to the p75 IL-2 receptor on LGL abrogated IL-2 induction of IL-1 beta mRNA, suggesting that IL-2 signaling via the p75 IL-2 receptor induced IL-1 beta gene expression in LGL.
Clark et al. (2000)IL-2NK cellsThese results indicate that local cationic lipid-mediated gene transfer of IL-2 induces activation of intratumoral NK cells and slows tumor growth.
Echevarria et al. (1991)IL2NK cellEnhanced NK cell activity appears to be secondary, at least in part, to increased production of IL2.
Nielsen et al. (1991)interleukin-2natural killer cellReduced natural killer cell activity and increased levels of soluble interleukin-2 receptors.
Hoyt et al. (1988)IL-2natural killer cellsSignificant T-cell changes in patients who developed sepsis include: decreased total T-cells, decreased helper cells, decreased natural killer cells, increased Ia expressing mononuclear cells, increased activated T-cells, (L22) and increased IL-2 expressing cells (TAC).
Waldmann and Goldman (1989)IL-2large granular lymphocytesThe p75 peptide is receptor for IL-2 on large granular lymphocytes and is sufficient for the IL-2 activation of these cells.
Biswas et al. (1997)IL-2NK cellThese observations suggest that in vitro human NK cell augmentation with analogs (1) and (2) reported earlier may be due to enhanced IL-2 production.
Chandra (1992)interleukin-2natural killer cellSubjects in the supplement group had higher numbers of certain T-cell subsets and natural killer cells, enhanced proliferation response to mitogen, increased interleukin-2 production, and higher antibody response and natural killer cell activity.
Payvandi et al. (2005)IL-2NK cellsTaken together, our results demonstrate that the IMiDs exert their effects at least in part by activating PKC-theta and acting on AP-1 DNA-binding activity in T cells, resulting in augmented IL-2 synthesis and activation of IL- 2-dependent downstream effectors, such as NK cells.
Miller et al. (1997)IL-2NK cellsIn vivo IL-2 primed NK cells obtained by lymphapheresis were activated in large-scale ex vivo incubation in high dose IL-2 (1,000 U/mL) at high cell density (10 x 10(6)/mL), in gas permeable bags, and using serum-free media.
Vitolo et al. (1993)IL-2NK cellsTo further characterize this subset of NK cells functionally, their potential to express mRNA for the IL-2R and various cytokines after IL-2 activation was examined.
Schmudde et al. (2010)IL-2NK cellsHowever, the HDI suberoylanilide hydroxamic acid (SAHA; vorinostat) interfered with the IL-2 activation of human NK cells and the priming of human tumour-specific T cells.
Perussia et al. (1987)IL-2NK cellsOur data indicate that proliferation of both T and NK cells is dependent upon IL-2 production in the culture, because an anti-IL-2 antiserum completely suppresses proliferation.
Umekage et al. (1998)IL-2natural killer cellsEnhancement by stem cell factor of interleukin-2 (IL-2)-induced DNA synthesis in human decidual CD16- CD56bright natural killer cells mediated by increased expression of the IL-2 receptor alpha chain.
Yu et al. (2000)IL-2NK cellsIL-2 activation of NK cells: involvement of MKK1/2/ERK but not p38 kinase pathway.
Wang et al. (2009)interleukin-2NK cellNaturally occurring CD4(+)CD25(+) T regulatory cells can inhibit NK cell cytotoxicity, while activated interleukin-2 (IL-2) secreting T cells can stimulate NK cells.
Shah et al. (2006)IL-2NK cellPURPOSE: Ultra low doses of interleukin-2 (IL-2) can activate the high-affinity IL-2 receptor constitutively expressed on CD56(bright) natural killer (NK) cells, the CD34+ NK cell precursor, and CD4+ CD25+ regulatory T cells (Tregs) in vivo.
Son et al. (2001)IL-2natural killer cellsPhenotypic analysis revealed a preferential expansion of CD56+CD3- cells and an up-regulation of IL-2 receptor-alpha expression on natural killer cells.
Sumitran et al. (1999)IL-2NK cellsHuman NK cells may thus contribute to a cellular rejection of pig neuronal xenografts by ADCC, or following IL-2 activation, by a direct cytotoxic effect.
Portevin et al. (2009)IL-2NK cellsWe propose that the higher proliferation status of NK cells when PBMCs are exposed to 3a-G1 (Fig. 1) is mainly due to an increase in the availability of IL-2 that has not been consumed by proliferating T cells.
Ramoni et al. (2002)IL-2natural killer cellsOnly ezrin changed its distribution following IL-2 activation and all three ezrin, moesin and radixin were polarized on uropods of adherent natural killer cells.
Ortaldo et al. (1984)IL 2LGLAll four preparations of IL 2 enhanced the cytotoxic activity of LGL without any detectable accessory requirement after incubation for as little as 6 hr, even though the MLA-144 IL 2 preparations were devoid of detectable interferons (IFN).
Ortaldo et al. (1984)IL 2LGLThe mechanism of IL 2 boosting appears to be a direct interaction with LGL, resulting in the production of IFN gamma.
Ortaldo et al. (1984)IL 2NK cellsIn parallel experiments, these same IL 2 preparations were quite active in causing the proliferation of T lymphocytes, clearly demonstrating a role of IL 2 in promoting the proliferation of NK cells as well as T cells.
Lister et al. (1995)rhIL-2NK cellsAdoptive transfer of A-NK cells and rhIL-2 during the pancytopenic phase after HDC-PBSCT was feasible and well tolerated, did not adversely affect engraftment, and resulted in amplified natural killer activity in the peripheral blood during the immediate posttransplantation period.
Casale et al. (1992)IL2NK cellsIn the present study, we assessed the effects of carbaryl (CA, an antiCHE insecticide) and alpha-naphthol (NA, the major metabolite of CA) on both target cell killing per se and IL2 enhancement of target cell killing by human NK cells.
Taga et al. (1996)IL-2NK cellsA proportion (15.2%) of NK cells that were stimulated for 3 days with IL-2 and then incubated for 4 hours with K562 cells showed rapid cell death, but NK cells not stimulated with IL-2 did not.
King et al. (1999)IL-2NK cellsCirculating CD56bright NK cells generally proliferate in the presence of interleukin-2 (IL-2), but it is clear that cofactors besides IL-2 are required for optimal response.
Malec et al. (1988)IL-2NK cellPRO significantly augmented spontaneous as well as PHA-stimulated IL-2 receptor expression, IL-2 generation, NK cell activity and AMLR observed at 30 and 150 min after the drug injection.
Hayward et al. (1986)IL-2NK cellsThe results indicate that NK cells contribute to the lysis of VZV infected cells and suggest that IL-2 release by T cells, as a result of HLA matching or antigen representation, may amplify this mechanism.
Herberman (1986)IL 2NK cellsWhen lymphocytes are cultured in the presence of interleukin 2 (IL 2), strong cytotoxic reactivity develops and it has been difficult to determine clearly the relationship of these effector cells to NK cells.
Voss et al. (1992)IL-2NK cellsIn a previous study of the IL-2 receptors expressed on NK cells obtained from cancer patients after in vivo IL-2 therapy, we documented a discrepancy between the level of beta chain and the level of intermediate-affinity IL-2 binding sites expressed on the cell surface.
Clark et al. (2000)IL-2natural killer cellsCationic lipid gene transfer of an IL-2 transgene leads to activation of natural killer cells in a SCID mouse human tumor xenograft.
Smyth and Ortaldo (1991)IL-2LGLIn particular, IL-6 did not stimulate detectable LGL IL-2 production or IL-2R modulation, and mAb to the p75 IL-2R had no effect on IL-6 induction of LGL NK activity.
Fuggetta et al. (2000)IL-2NK cellsMoreover, the exposure of mononuclear cells to HY before IL-2 stimulation did not affect the generation of IL-2-activated NK cells, whereas, the hyperthermic treatment of IL-2-activated NK cells produced a marked reduction of their cytotoxic activity.
Voss et al. (1990)interleukin 2natural killer cellsIncreased expression of the interleukin 2 (IL-2) receptor beta chain (p70) on CD56+ natural killer cells after in vivo IL-2 therapy: p70 expression does not alone predict the level of intermediate affinity IL-2 binding.
Grob et al. (1988)interleukin 2natural killer cellsData are given here showing that after such events the levels of immunoglobulins; the complement factors C3C, C4 and C Factor B; and the numbers of circulating lymphocytes and of the subpopulations CD3, CD4, CD8 and natural killer cells as well as the stimulatory capacity of mononuclear cells to mitogen fall; while the levels of acute phase proteins, neopterin and interleukin 2 receptors and the spontaneous uptake of thymidine by mononuclear cells become augmented.
Downing and Taylor (1987)interleukin-2natural killer cellIn order to determine whether hyperthermia was associated with other immunostimulatory effects, we measured lymphocyte activation, natural killer cell activity, interleukin-2 (IL-2) production and endotoxin-induced tumor necrosis factor (TNF) activity in blood samples obtained from normothermic (37 degrees C) and hyperthermic (39 degrees C) individuals.
Kasahara et al. (1983)IL 2LGLFurther analysis of cells in the LGL population using various monoclonal antibodies revealed that removal of cells with OKT11 or AF-10, a monoclonal antibody against human HLA-DR antigen, decreased IL 2 production, whereas removal of OKT8+, OKM1+, Leu-M1+, or Leu-7+ cells led to enhanced IL 2 production.
Nagaraj et al. (2004)IL-2NK cellIL-2 secretion by the CIK cells enhances the NK cell antitumor activity [20].
London et al. (1986)IL 2NK cellsIL 2 is a growth factor for both cell types, but although the presence of the growth factor is sufficient for quiescent NK cells to be induced into cycle, T cells require antigenic or other mitogenic stimuli to respond to IL 2.
Weigent et al. (1983)IL 2NK cellSpecific antibodies either to natural IFN-gamma or to a synthetic peptide corresponding to the human IFN-gamma N-terminal amino acids, when added to cultures treated with IL 2, completely blocked IL 2 enhancement of NK cell activity for both the mouse and human systems.
Martin et al. (2010)IL-2NK cellWe hypothesized that this unexpected expansion is paradoxically IL-2 driven; caused by the increased availability of T cell-derived IL-2 for NK cell signaling.
Martin et al. (2010)IL-2-drivenNK cellsAn IL-2 paradox: blocking CD25 on T cells induces IL-2-driven activation of CD56(bright) NK cells.
Vitte-Mony et al. (1994)IL-2natural killer cellWe show here, using IL-2-dependent human natural killer cell lines, that p56lck is regulated by IL-2 in two different ways: (1) IL-2 induces a rapid increase of p56lck kinase activity as assessed in vitro; and (2) following IL-2 stimulation, p56lck undergoes phosphorylation on serine residues that is reflected by a modification of its electrophoretic mobility in SDS-PAGE.
Vitte-Mony et al. (1994)IL-2NK cellFurthermore, pp120 was identified as rasGAP, by Western blot and immunoprecipitation experiments. rasGAP and some of its co-precipitating molecules become phosphorylated in response to IL-2, presumably by p56lck, which would thus provide a link between IL-2R and downstream events critical for NK cell proliferation and function.
Vitte-Mony et al. (1994)interleukin 2natural killer cellsSignal transduction of interleukin 2 in human natural killer cells: involvement of the p56lck tyrosine kinase.
Dybkaer et al. (2007)IL2NK cellsWe also observed a change in the expression profile of transcripts on this pathway on IL2 activation with downregulation of many of the transcripts mentioned above and upregulation of receptors (TGFBR1,TGFBR2 and TGFBR3) and the R-SMAD (SMAD2) in activated NK cells.
Dybkaer et al. (2007)IL2NK cellsUpon IL2 stimulation of NK cells, signal transduction from tyrosine phosphorylation of the IL2R?
Savary et al. (1989)IL-2LGLAdditionally, the rate of tumor cell killing and the recycling capacity of LGL were substantially increased (63-76-fold and 4-9-fold, respectively), following IL-2 activation.
Bruunsgaard et al. (2001)interleukin-2NK cellsCa(2+) independent cytotoxicity was unaltered, and NK cells maintained their cytotoxic responses to interleukin-2 and interferon-alpha signals.
Hellstrand and Hermodsson (1990)IL-2NK cellsAddition of peripheral-blood monocytes, recovered by countercurrent centrifugal elutriation, to purified NK cells abrogated IL-2 induced NK cell activation, reconstituted the synergistic, NK-activating effects of histamine and IL-2, and strongly reduced baseline NKCC.
Edsparr et al. (2010)IL-2NK cellsWe furthermore found that freshly isolated human NK cells Matrigel invasion was MMP-dependent and it increased in response to IL-2.
Sconocchia et al. (1999)IL-2NK cellsFresh NK cells acquired CD38-dependent lytic function during activation with interleukin-2 (IL-2), and inhibitor studies suggested that IL-2 stimulated the de novo expression of proteins that act between CD38 and the lytic machinery in NK cells.
Bhat and Watzl (2007)IL-2NK cellUsing functional assays, we demonstrate that on an average, a single IL-2 activated NK cell can kill four target cells.
Takahashi et al. (2009)IL-2NK cellsTaken together, the results of the previous investigation and those of this study show that repeated elevation of IL-2 (although it immediately returned to the baseline level) causes chronic and recurrent stimulation to NK cells and results in the steady activation of NK cells.
Grzywacz et al. (2002)IL-2NK cellsNK cells become Ki-67+ in MLC and expand depending on the lack of ligand for KIR on stimulator cells in IL-2 supplemented MLC.
Conti et al. (1992)IL-2NK cellsThese studies provide new evidence of the biological potential of IL-1ra since this new protein enhances IL-2 activity on NK cells.
Yamauchi and Bloom (1993)IL-2-inducedNK cellsIn the presence of L-buthionine-(S,R)-sulfoximine, an inhibitor of GSH synthesis, IL-2-induced LAK activity and proliferation of NK cells in medium without L-cystine and GSH, could be restored, at least in part, by addition of GSH, but not 2-ME or L-cystine.
Echevarria et al. (1991)IL2NK cellWhen patients were divided in accordance with markers of HBV replication, HBV-DNA positive patients showed increased NK cell activity and IL2 levels as compared with the control group, whereas in HBV-DNA-negative patients no differences were found.
Vlk et al. (2000)IL-2NK cellT and, more markedly, NK cell proliferation, induction of activation markers on the surface of T and NK subsets, and elevation of sIL-2R alpha concentrations were seen in the IL-2 + IFN alpha subgroup.
Lotzová et al. (1987)interleukin 2NK cellInduction of NK cell activity against fresh human leukemia in culture with interleukin 2.
Umehara and Bloom (1990)IL-2large granular lymphocytesThe IL-2 receptor beta subunit is absolutely required for mediating the IL-2-induced activation of NK activity and proliferative activity of human large granular lymphocytes.
Nagaraj et al. (2004)IL-2 cytokine genenatural killer cellsIn this regard, adenoviral-mediated expression of IL-2 cytokine gene in several tumor models has been found to induce strong and specific antitumor responses [18] by stimulating immune cells including T and natural killer cells.
Bhat et al. (2007)IL-2NK cellsFresh NK cells were stimulated without feeder cells in the presence of IL-2 (100 IU/ml) (NIH cytokine repository), IL-15 (10 ng/ml) (R&D systems, Wiesbaden, Germany) and IFN-?
Bhat et al. (2007)IL-2NK cellsHowever, the killing ability of these ‘exhausted’ NK cells was augmented in response to IL-2 treatment on day 2 and was similar to that of control NK cells (Fig. 4B).
Bhat et al. (2007)IL-2NK cellsIn the experiments described above we used primary human NK cells, which had been expanded in the presence of IL-2 for 2 weeks, as such cells showed a high cytotoxic activity.
Phillips et al. (1989)IL-2NK cellsCollectively, results from the present studies directly implicate the p75 IL-2R as the structure predominantly responsible for IL-2 activation of NK cells.
Robertson et al. (1993)IL-2NK cellsNevertheless, CD56dim NK cells proliferate poorly in response to IL-2 alone.
Lotzová et al. (1993)IL-2NK cellsGeneration of cytotoxic NK cells in LTBMC was dependent on the dose of IL-2; although CD56+CD3- NK cells were generated in LTBMC supplemented with a broad range of doses (10 to 10(3) U/ml) of IL-2, the acquisition of full cytotoxic function required a high concentration of IL-2 (10(3) U/ml).
Warren et al. (1993)IL-2NK cellCompared with IL-2-CM, rIL-2 was an inefficient costimulator for the induction of NK cell proliferation, suggesting that factors in IL-2-CM were required in addition to IL-2, but rIL-2 was as efficient as IL-2-CM in maintaining the proliferation of activated NK cells.
Umekage et al. (1998)IL-2NK cellsAlthough SCF alone had no effect on DNA synthesis in decidual CD16- CD56bright NK cells, it enhanced the proliferative effect of interleukin-2 (IL-2) at IL-2 concentrations that selectively saturate the high-affinity IL-2 receptor (IL-2R).