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PMID |
Sentence |
| 1 |
2056245
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Developmental regulation of the cytokine repertoire in human macrophages: IL-1, IL-6, TNF-alpha, and M-CSF.
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| 2 |
2056245
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For each of the cytokines tested, interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, and macrophage colony-stimulating factor (M-CSF), a different pattern of regulation was observed.
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| 3 |
2056245
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From the LPS-dependent cytokines, IL-1 beta and IL-6 were downregulated whereas TNF-alpha levels increased severalfold.
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| 4 |
2056245
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For the release of IL-1 beta, IL-6, and TNF-alpha a synergistic effect of interferon-gamma (IFN-g) and lipopolysaccharide (LPS) was observed.
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| 5 |
2056245
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Upon further cultivation of MAC up to 28 days, LPS-induced IL-1 beta levels remained very low, but IL-6 levels increased again reaching that of blood MO, and TNF-alpha continued to rise reaching levels up to 30-fold higher than in blood MO.
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| 6 |
2056245
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Long-term cultured MAC started to release IL-6 and TNF-alpha also in the absence of a stimulus and, furthermore, became responsive to IFN-g alone.
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| 7 |
2056245
|
Developmental regulation of the cytokine repertoire in human macrophages: IL-1, IL-6, TNF-alpha, and M-CSF.
|
| 8 |
2056245
|
For each of the cytokines tested, interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, and macrophage colony-stimulating factor (M-CSF), a different pattern of regulation was observed.
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| 9 |
2056245
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From the LPS-dependent cytokines, IL-1 beta and IL-6 were downregulated whereas TNF-alpha levels increased severalfold.
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| 10 |
2056245
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For the release of IL-1 beta, IL-6, and TNF-alpha a synergistic effect of interferon-gamma (IFN-g) and lipopolysaccharide (LPS) was observed.
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| 11 |
2056245
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Upon further cultivation of MAC up to 28 days, LPS-induced IL-1 beta levels remained very low, but IL-6 levels increased again reaching that of blood MO, and TNF-alpha continued to rise reaching levels up to 30-fold higher than in blood MO.
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| 12 |
2056245
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Long-term cultured MAC started to release IL-6 and TNF-alpha also in the absence of a stimulus and, furthermore, became responsive to IFN-g alone.
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| 13 |
8018827
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Expression of lymphokine genes including interleukin 2 (IL-2), interleukin 3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon gamma (IFN-g), tumor necrosis factor (TNF) and lymphotoxin (LT) were sequentially monitored in peripheral blood mononuclear cells by Northern blot analysis after stimulation with phytohemagglutinin (PHA).
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| 14 |
8018827
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Lymphokines including IL-2, IL-3 and GM-CSF belong to type 1 and IFN-g, TNF and LT belong to type 2.
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| 15 |
8972688
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Comparison of granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor and interferon-gamma.
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| 16 |
8972688
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Oxidative burst response upon stimulation with N-formyl-methionyl-leucyl-phenylalanine was assessed in neutrophils after priming with granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and interferon-gamma (IFN-g), and in monocytes after priming with GM-CSF and IFN-g.
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| 17 |
8972688
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In contrast, following priming with IFN-g, GM-CSF or medium (but not G-CSF) the neutrophils in HIV patients with CD4 counts > 200 x 10(9)/L exhibited a significantly higher chemiluminescence response than was seen in healthy age-matched controls, whereas the response in patients with lower CD4 counts was not different from controls.
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| 18 |
8972688
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At comparable concentrations, GM-CSF induced a significantly higher priming than G-CSF and IFN-g.
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| 19 |
8972688
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A significant positive correlation between CD4 counts and priming activity of GM-CSF and IFN-g on neutrophils was observed.
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| 20 |
8972688
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Comparison of granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor and interferon-gamma.
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| 21 |
8972688
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Oxidative burst response upon stimulation with N-formyl-methionyl-leucyl-phenylalanine was assessed in neutrophils after priming with granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and interferon-gamma (IFN-g), and in monocytes after priming with GM-CSF and IFN-g.
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| 22 |
8972688
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In contrast, following priming with IFN-g, GM-CSF or medium (but not G-CSF) the neutrophils in HIV patients with CD4 counts > 200 x 10(9)/L exhibited a significantly higher chemiluminescence response than was seen in healthy age-matched controls, whereas the response in patients with lower CD4 counts was not different from controls.
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| 23 |
8972688
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At comparable concentrations, GM-CSF induced a significantly higher priming than G-CSF and IFN-g.
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| 24 |
8972688
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A significant positive correlation between CD4 counts and priming activity of GM-CSF and IFN-g on neutrophils was observed.
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| 25 |
18006399
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Gene expression of RANKL, OPG, TGFB2, IFNG and CSF-1 was analyzed after no mechanical stimulation (control), exposure to compression or exposure to micromotions.
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| 26 |
18006399
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We observed an 8-fold upregulation of RANKL after exposure to micromotions, and downregulation of OPG, IFNG and TGFB2.
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| 27 |
18006399
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The RANKL:OPG ratio was upregulated 24-fold after micromotions.
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| 28 |
18653623
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Insulin-like growth factor-1 delays Fas-mediated apoptosis in human neutrophils through the phosphatidylinositol-3 kinase pathway.
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| 29 |
18653623
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We previously showed that insulin-like growth factor-1 (IGF1) delays spontaneous neutrophil apoptosis without influencing the secretion of cytokines by these cells.
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| 30 |
18653623
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We show that IGF1 delays neutrophil apoptosis triggered by the agonistic anti-Fas antibody CH11 and that the effect of IGF1 is comparable in magnitude to that of the acknowledged anti-apoptotic cytokines interferon-gamma (IFNG) and granulocyte-macrophage colony-stimulating factor (GM-CSF; now known as CSF2).
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| 31 |
18653623
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IGF1 did not affect Fas expression or activation by anti-Fas of caspase-8, but inhibited the depolarization of the mitochondrial membrane.
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| 32 |
18653623
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Inhibitor studies indicate that the phosphatidylinositol-3 kinase (PI3K) pathway, but not the MEK-ERK pathway, mediates the effects of IGF1.
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| 33 |
18653623
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However, in contrast to CSF2, IGF1 did not induce phosphorylation and translocation to the membrane of AKT, the canonical downstream target of PI3K.
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| 34 |
18653623
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We therefore speculate that other downstream targets of PI3K are involved in the delay of neutrophil apoptosis by IGF1, possibly through stabilization of the mitochondrial membrane.
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| 35 |
19578489
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We identified 7 proteins that significantly differentiate HCC patients from hepatitis patients (p < 0.05) (AFP, CTNNB, CSF1, SELL, IGFBP6, IL6R, and VCAM1).
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| 36 |
19578489
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Importantly, we also identified 8 proteins that significantly differentiate HCC patients with 'normal' levels of AFP (< 20 ng/ml) from hepatitis patients (p < 0.05) (IL1RN, IFNG, CDKN1A, RETN, CXCL14, CTNNB, FGF2, and SELL).
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| 37 |
20093719
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It has been defined that mast cells express TLR2, TLR4, TLR1 and TLR6.
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| 38 |
20093719
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There is also some data proving that mast cells possess TLR5, TLR3 and TLR9 molecules.
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| 39 |
20093719
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The presence of TLR7, TLR9, and TLR10 on mast cells is still unclear.
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| 40 |
20093719
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Some data indicate that TLR expression by mast cells can be modulated by various cytokines, such as granulocyte-macrophage colony stimulating factor (GM-CSF) and interferon (IFN)-g, cathelicidin LL-37 as well as by some bacterial components.
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| 41 |
23566200
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Mϕs differentiated with macrophage colony-stimulating factor and interferon-γ (Mγ-Mϕs), which are similar to the human intestinal lamina propria CD14(+) Mϕs that contribute to Crohn's disease (CD) pathogenesis by production of pro-inflammatory cytokines, highly expressed TGR5 compared with any other type of differentiated Mϕ and dendritic cells.
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| 42 |
23566200
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Among LPMCs, isolated CD14(+) intestinal Mϕs from patients with CD expressed TGR5.
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| 43 |
23566200
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In isolated intestinal CD14(+) Mϕs, a TGR5 agonist could inhibit tumour necrosis factor-α production.
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