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PMID |
Sentence |
1 |
11223078
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We demonstrate that FPH22.PSA targeted PSA was internalized and processed by the human myeloid THP-1 cell line resulting in presentation of MHC class I-associated PSA peptides and lysis of THP-1 by PSA-specific human CTL.
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2 |
11895951
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To understand the mechanism(s) implicated in the regulation of the synthesis and release of IL-10 during early infection, we investigated the autocrine effects of IL-6, IL-12, tumor necrosis factor alpha (TNF-alpha), and IL-10 itself, as well as the exocrine effect of IFN-gamma on the production of macrophage-derived IL-10 with lipoprotein as a stimulant.
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3 |
11895951
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TNF-alpha increased the production of IL-10, as elicited by lipoproteins.
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4 |
11895951
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The production of IL-10 by THP-1 cells stimulated with L-OspA was autoregulated by a negative feedback mechanism involving the IL-10 receptor (IL-10R).
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5 |
11895951
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Exogenous IFN-gamma significantly inhibited the production of IL-10.
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6 |
11895951
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Both autocrine (IL-10) and exocrine (IFN-gamma) inhibition of IL-10 production resulted in an increase in the production of the proinflammatory cytokines IL-6 and IL-12.
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7 |
17517859
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Nineteen out of 22 OMP-1/P28 family proteins, including P28 (which previously was shown to be surface exposed), were detected in E. chaffeensis cultured in human monocytic leukemia THP-1 cells.
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8 |
19793902
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Mycoplasma genitalium-derived lipid-associated membrane proteins activate NF-kappaB through toll-like receptors 1, 2, and 6 and CD14 in a MyD88-dependent pathway.
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9 |
19793902
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However, the interaction of M. genitalium-derived LAMPs as pathogenic agents with Toll-like receptors (TLRs) and the signaling pathways responsible for active inflammation and NF-kappaB activation have not been fully elucidated.
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10 |
19793902
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In this study, LAMPs induced the production of tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) in a dose-dependent manner.
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11 |
19793902
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Blocking assays showed that TLR2- and CD14-neutralizing antibodies reduced the expression of TNF-alpha and IL-6 in THP-1 cells.
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12 |
19793902
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Furthermore, LAMP-induced NF-kappaB activation was increased in 293T cells transfected with TLR2 plasmid.
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13 |
19793902
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The activity of NF-kappaB was synergically augmented by cotransfected TLR1, TLR6, and CD14.
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14 |
19793902
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Additionally, LAMPs were shown to inhibit NF-kappaB expression by cotransfection with dominant-negative MyD88 and TLR2 plasmids.
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15 |
19793902
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These results suggest that M. genitalium-derived LAMPs activate NF-kappaB via TLR1, TLR2, TLR6, and CD14 in a MyD88-dependent pathway.
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16 |
20417300
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In this paper, we studied the immunostimulatory activity of the recombinant BCG strains in vitro and found out that rBCG-A(N)-E-A(C) activated THP-1 cells and induced higher expression levels of CD86, CD80, CD40 and HLA-DR, especially increased the ratio of CD86/CD80.
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17 |
20417300
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Moreover, rBCG-A(N)-E-A(C) up-regulated the expression of EFHD2, ACTB and ACTG1 in the macrophages and improved the ability of antigen presentation and the CD8(+) T-cells immune response.
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18 |
23507086
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Molecular pathways upregulated by MA-CNTs included IL6, CD40, dendritic cell maturation, tumor necrosis factor-(TNF)-α/TNFR1-2, NFKB signaling and T helper 1 chemokine pathways (CXCR3 and CCR5 ligand pathways).
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19 |
23507086
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To confirm the results at protein level, the secretion of IL1β, TNFα, IL6 and IL10 by THP1 and primary monocytes was assessed by ELISA, corroborating gene-expression data.
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20 |
23536693
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Mycoplasma fermentans MALP-2 induces heme oxygenase-1 expression via mitogen-activated protein kinases and Nrf2 pathways to modulate cyclooxygenase 2 expression in human monocytes.
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21 |
23536693
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Specific inhibitors of mitogen-activated protein kinases (MAPKs), SB203580, PD98059, and SP600125, significantly abolished HO-1 expression.
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22 |
23536693
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In addition, MALP-2 also induced NF-E2-related factor 2 (Nrf2) translocation, and the silencing of Nrf2 expression in THP-1 cells decreased the levels of MALP-2-mediated HO-1 expression.
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23 |
23536693
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Furthermore, COX-2 protein expression levels were upregulated in THP-1 cells in response to MALP-2, and transfection with small interfering RNAs of HO-1 significantly increased COX-2 accumulation.
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24 |
23536693
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These results demonstrate that MALP-2 induces HO-1 expression via MAPKs and Nrf2 pathways and, furthermore, that MALP-2-induced COX-2 expression was modulated by HO-1 in THP-1 cells.
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25 |
24093105
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Moreover, EDAvidin retains the proinflammatory properties of EDA, inducing NF- κβ by TLR4-expressing cells, as well as the production of TNF- α by the human monocyte cell line THP1 and IL-12 by DC.
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26 |
24467650
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Stimulation of THP-1 macrophages with recombinant PE35 and PPE68, singly or in combination, led to a dose-dependent increase in levels of the anti-inflammatory cytokine interleukin (IL)-10 and the chemokine monocyte chemoattractant protein-1, and caused a reciprocal decrease in levels of the proinflammatory cytokine IL-12.
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27 |
24467650
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PE35/PPE68-stimulated production of IL-10 and monocyte chemoattractant protein-1 was observed to be dependent on toll-like receptor 2, as receptor blockade caused a significant reduction in their levels.
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28 |
26225923
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Interleukin-24 (IL-24), a member of the IL-10 cytokine gene family, causes growth suppression and apoptosis in various solid tumor cells.
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29 |
26225923
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In addition, IL-24 expression could significantly induce apoptosis of the THP-1 cells.
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30 |
26225923
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Ad.RGD-IL-24 had a potent effect on the up-regulation of the expression of GRP78/Bip, GADD34 and Bax, down-regulation of the expression of Bcl-2 and Mcl-1, and induced the activation of Caspase-3, which may be responsible for its apoptosis-inducing effect on THP-1 cells.
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31 |
26225923
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Interleukin-24 (IL-24), a member of the IL-10 cytokine gene family, causes growth suppression and apoptosis in various solid tumor cells.
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32 |
26225923
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In addition, IL-24 expression could significantly induce apoptosis of the THP-1 cells.
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33 |
26225923
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Ad.RGD-IL-24 had a potent effect on the up-regulation of the expression of GRP78/Bip, GADD34 and Bax, down-regulation of the expression of Bcl-2 and Mcl-1, and induced the activation of Caspase-3, which may be responsible for its apoptosis-inducing effect on THP-1 cells.
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