PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2839482-3 1988 During cell incubation with TNF receptor degradation suppressed by chloroquine, the number of surface TNF receptors remained approximately constant, but the total number of surface and internal TNF receptors increased gradually, at 3 h reaching 1.5 times the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. Chloroquine 67-78 tumor necrosis factor Homo sapiens 28-31 2839482-3 1988 During cell incubation with TNF receptor degradation suppressed by chloroquine, the number of surface TNF receptors remained approximately constant, but the total number of surface and internal TNF receptors increased gradually, at 3 h reaching 1.5 times the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. Chloroquine 67-78 tumor necrosis factor Homo sapiens 102-105 2839482-3 1988 During cell incubation with TNF receptor degradation suppressed by chloroquine, the number of surface TNF receptors remained approximately constant, but the total number of surface and internal TNF receptors increased gradually, at 3 h reaching 1.5 times the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. Chloroquine 67-78 tumor necrosis factor Homo sapiens 102-105 2839482-3 1988 During cell incubation with TNF receptor degradation suppressed by chloroquine, the number of surface TNF receptors remained approximately constant, but the total number of surface and internal TNF receptors increased gradually, at 3 h reaching 1.5 times the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. Chloroquine 67-78 tumor necrosis factor Homo sapiens 102-105 32382733-1 2020 On human lung parenchymal explants, chloroquine concentration clinically achievable in the lung (100 muM) inhibited the lipopolysaccharide-induced release of TNF-alpha (by 76%), IL-6 (by 68%), CCL2 (by 72%) and CCL3 (by 67%). Chloroquine 36-47 tumor necrosis factor Homo sapiens 158-167 2829746-3 1988 During cell incubation with suppression of TNF receptor degradation by chloroquine, the number of surface TNF receptors remained approximately constants, but the total number of surface and internal TNF receptors increased gradually, at 3h reaching 1.5 times of the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. Chloroquine 71-82 tumor necrosis factor Homo sapiens 43-46 2829746-3 1988 During cell incubation with suppression of TNF receptor degradation by chloroquine, the number of surface TNF receptors remained approximately constants, but the total number of surface and internal TNF receptors increased gradually, at 3h reaching 1.5 times of the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. Chloroquine 71-82 tumor necrosis factor Homo sapiens 106-109 2829746-3 1988 During cell incubation with suppression of TNF receptor degradation by chloroquine, the number of surface TNF receptors remained approximately constants, but the total number of surface and internal TNF receptors increased gradually, at 3h reaching 1.5 times of the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. Chloroquine 71-82 tumor necrosis factor Homo sapiens 106-109 2829746-3 1988 During cell incubation with suppression of TNF receptor degradation by chloroquine, the number of surface TNF receptors remained approximately constants, but the total number of surface and internal TNF receptors increased gradually, at 3h reaching 1.5 times of the initial number, thus suggesting continuous synthesis, externalization, internalization, and degradation of the TNF receptor in the absence of cycloheximide. Chloroquine 71-82 tumor necrosis factor Homo sapiens 106-109 32694530-8 2020 TNFA and IL10 expressions significantly decreased after 48 h (p < 0.001) and 24 h (p < 0.002), respectively, by both CQ and CQ NPs treatment. Chloroquine 117-119 tumor necrosis factor Homo sapiens 0-4 32787548-5 2020 Then, levels of autophagy-related proteins and inflammation-related proteins (TNF-alpha, IL-Ibeta) were detected, indicating that Chloroquine and Sirtinol reversed the protective effect of H2S on SH-SY5Y cells induced by MPP~+. Chloroquine 130-141 tumor necrosis factor Homo sapiens 78-87 32920000-6 2020 Chloroquine/hydroxychloroquine + azithromycin interacted with 6 genes (CCL2, CTSB, CXCL8, IL1B, IL6 and TNF), whereas chloroquine and azithromycin affected two additional genes (BCL2L1 and CYP3A4), which might be a reason behind a greater number of consequential diseases. Chloroquine 0-11 tumor necrosis factor Homo sapiens 104-107 32920000-6 2020 Chloroquine/hydroxychloroquine + azithromycin interacted with 6 genes (CCL2, CTSB, CXCL8, IL1B, IL6 and TNF), whereas chloroquine and azithromycin affected two additional genes (BCL2L1 and CYP3A4), which might be a reason behind a greater number of consequential diseases. Chloroquine 19-30 tumor necrosis factor Homo sapiens 104-107 32920000-7 2020 In contrast to lopinavir/ritonavir, chloroquine/hydroxychloroquine + azithromycin downregulated the expression of TNF and IL6. Chloroquine 36-47 tumor necrosis factor Homo sapiens 114-117 33062720-3 2020 Also, CQ and HCQ inhibit the production of interferon- (IFN-) alpha and IFN-gamma and/or tumor necrotizing factor- (TNF-) alpha. Chloroquine 6-8 tumor necrosis factor Homo sapiens 89-127 32694530-8 2020 TNFA and IL10 expressions significantly decreased after 48 h (p < 0.001) and 24 h (p < 0.002), respectively, by both CQ and CQ NPs treatment. Chloroquine 124-126 tumor necrosis factor Homo sapiens 0-4 23482646-5 2013 Chloroquine exerted a direct pH-dependent antifungal effect on Aspergillus fumigatus and Aspergillus nidulans; it increased the antifungal activity of PMNs from patients with CGD at a significantly lower concentration, compared with the concentration for PMNs from healthy individuals; and decreased the hyperinflammatory state of PBMCs from patients with CGD, as observed by decreased tumor necrosis factor alpha and interleukin 1beta release. Chloroquine 0-11 tumor necrosis factor Homo sapiens 386-413 29061481-7 2018 Furthermore, CQ pretreatment exacerbated palmitate-induced TNF-alpha and IL-6 mRNA expression in PBMCs. Chloroquine 13-15 tumor necrosis factor Homo sapiens 59-68 25721154-3 2015 In this cross-sectional study, we investigated the association of MIF and TNFalpha serum levels with methotrexate (MTX) and in combination with chloroquine (CLQ) and sulfasalazine (SSZ) in RA patients classified according to the ACR/EULAR 2010 criteria. Chloroquine 157-160 tumor necrosis factor Homo sapiens 74-82 25721154-7 2015 Furthermore, we subclassified 97 patients with established RA (>=2 years of disease duration) and found that TNFalpha serum levels were lower in the combination therapy group (MTX + CLQ + SSZ) in comparison with the monotherapy MTX group (16.7 pg/mL versus 13.6 pg/mL, p = 0.02). Chloroquine 185-188 tumor necrosis factor Homo sapiens 112-120 24680477-9 2014 On the other hand, the analysis of the antimalarial effect showed that chloroquine was able to inhibit in vitro the expression of TNFalpha and STAT4 enhanced by IFNalpha. Chloroquine 71-82 tumor necrosis factor Homo sapiens 130-138 24680477-11 2014 CONCLUSIONS: IFNalpha treatment enhances the induction of TNFalpha and STAT4 in stimulated monocytes, an effect inhibited in vitro by chloroquine treatment. Chloroquine 134-145 tumor necrosis factor Homo sapiens 58-66 22638980-0 2012 Differential effects of the autophagy inhibitors 3-methyladenine and chloroquine on spontaneous and TNF-alpha-induced neutrophil apoptosis. Chloroquine 69-80 tumor necrosis factor Homo sapiens 100-109 22638980-6 2012 Unexpectedly, both MA and CQ significantly delayed neutrophil apoptosis induced by TNF-alpha, although the inhibitors did attenuate late pro-survival effect of the cytokine. Chloroquine 26-28 tumor necrosis factor Homo sapiens 83-92 19783825-2 2009 In this report, we demonstrate that submicron particles (800-900 nm) composed of the polyketal PK3 and chloroquine, termed as the PKCNs, can deliver tumor necrosis factor-alpha (TNF-alpha) siRNA in vivo to Kupffer cells efficiently and inhibit gene expression in the liver at concentrations as low as 3.5 microg/kg. Chloroquine 103-114 tumor necrosis factor Homo sapiens 178-187 21691053-8 2012 Endosomal TLR3 inhibition by chloroquine dose-dependently inhibited dsRNA-induced TSLP generation and reduced generation of CXCL8, TNF-alpha, and IFN-beta. Chloroquine 29-40 tumor necrosis factor Homo sapiens 131-140 20386869-8 2010 TNF production in LPS/IFNgamma-activated monocytes was readily downregulated by dexamethasone and, to some extent, by chloroquine and etanercept. Chloroquine 118-129 tumor necrosis factor Homo sapiens 0-3 20089705-4 2010 Dependence on TLR was supported by the significant inhibition of TNF-alpha release by IRS661 and chloroquine. Chloroquine 97-108 tumor necrosis factor Homo sapiens 65-74 19783825-2 2009 In this report, we demonstrate that submicron particles (800-900 nm) composed of the polyketal PK3 and chloroquine, termed as the PKCNs, can deliver tumor necrosis factor-alpha (TNF-alpha) siRNA in vivo to Kupffer cells efficiently and inhibit gene expression in the liver at concentrations as low as 3.5 microg/kg. Chloroquine 103-114 tumor necrosis factor Homo sapiens 149-176 18953633-7 2009 Although CpG-ODN had no significant effect on the IL-6 production, it was able to induce the increase of TNF-alpha protein expression and this effect was inhibited by CHQ pretreatment. Chloroquine 167-170 tumor necrosis factor Homo sapiens 105-114 18764842-2 2008 OBJECTIVES: The aim of this study was to evaluate whether 3 months of monotherapy with chloroquine influences the mRNA skin expression of interleukin (IL)-1beta, IL-6 and tumour necrosis factor-alpha (TNF-alpha) in nonirradiated and locally ultraviolet B (UVB) irradiated nondiseased skin of patients with systemic lupus erythematosus (SLE). Chloroquine 87-98 tumor necrosis factor Homo sapiens 201-210 19017992-5 2008 This suggested a role for these TLRs in production of TNF and IL-6 from RA which was supported by data from chloroquine, an inhibitor of endosomal acidification (a prerequisite for TLRs 3, 7, 8, and 9 activation) which also inhibited production of these cytokines from RA synovial cultures. Chloroquine 108-119 tumor necrosis factor Homo sapiens 54-57 18764842-7 2008 Significantly lower expression of IL-1beta, IL-6 and TNF-alpha mRNAs was noted in irradiated skin samples after 3 months of chloroquine treatment. Chloroquine 124-135 tumor necrosis factor Homo sapiens 53-62 16670522-10 2006 The addition of chloroquine abolished the inhibitory effects of ISS-ODNs on colonic TNF-alpha and IL-1beta generation. Chloroquine 16-27 tumor necrosis factor Homo sapiens 84-93 16870179-4 2006 The endosomal acidification inhibitors, chloroquine or bafilomycin A, inhibited CpG ODN-induced TNF-alpha, TNFR-II, and MMP-9 expression. Chloroquine 40-51 tumor necrosis factor Homo sapiens 96-105 16418198-2 2006 The anti-rheumatic drug chloroquine has been shown to inhibit TNF-alpha, IL-1 and IL-6 production from mononuclear phagocytes. Chloroquine 24-35 tumor necrosis factor Homo sapiens 62-71 16418198-8 2006 RESULTS: TNF-alpha release from the cells was inhibited by chloroquine, whereas the steady-state level of TNF-alpha mRNA and synthesis of 26-kDa TNF-alpha precursor were not changed by chloroquine. Chloroquine 59-70 tumor necrosis factor Homo sapiens 9-18 16418198-12 2006 CONCLUSIONS: Our results indicate that chloroquine-mediated inhibition of TNF-alpha, IL-1beta and IL-6 synthesis occurs through different modes in lipopolysaccharide-stimulated human monocytes/macrophages: it blocks the conversion of cell-associated TNF-alpha precursor to mature soluble protein, whereas it reduces the levels of IL-1beta and IL-6 mRNA, at least in part, by decreasing their stability and by a pH-dependent mechanism. Chloroquine 39-50 tumor necrosis factor Homo sapiens 74-83 16418198-12 2006 CONCLUSIONS: Our results indicate that chloroquine-mediated inhibition of TNF-alpha, IL-1beta and IL-6 synthesis occurs through different modes in lipopolysaccharide-stimulated human monocytes/macrophages: it blocks the conversion of cell-associated TNF-alpha precursor to mature soluble protein, whereas it reduces the levels of IL-1beta and IL-6 mRNA, at least in part, by decreasing their stability and by a pH-dependent mechanism. Chloroquine 39-50 tumor necrosis factor Homo sapiens 250-259 16418198-0 2006 Chloroquine inhibits production of TNF-alpha, IL-1beta and IL-6 from lipopolysaccharide-stimulated human monocytes/macrophages by different modes. Chloroquine 0-11 tumor necrosis factor Homo sapiens 35-44 16447232-8 2006 Finally, CQ-resistant CEM cells displayed a markedly reduced capacity to release proinflammatory cytokines (tumor necrosis factor alpha) and chemokines (interleukin-8). Chloroquine 9-11 tumor necrosis factor Homo sapiens 108-135 16761500-7 2006 After three-months of chloroquine therapy the mean level of IL-6, IL-18 and TNF-alpha decreased significantly. Chloroquine 22-33 tumor necrosis factor Homo sapiens 76-85 14996414-7 2004 In human peripheral blood mononuclear cells (hPBMC), 100-200 microM CQ almost completely abrogated release of both TNF-alpha and IL-6 induced by CpG ODN and LPS, whereas IL-6 release induced by EC DNA was not significantly affected by 50 microM CQ. Chloroquine 68-70 tumor necrosis factor Homo sapiens 115-124 15854645-5 2005 The induction of TNF-alpha, IL-6 and interferon alpha (IFN-alpha) was chloroquine-sensitive and dependent more likely on endosomal Toll-like receptor signaling in particular TLR8. Chloroquine 70-81 tumor necrosis factor Homo sapiens 17-26 15031635-3 2003 GST and CQ were equally effective in reducing lipopolysaccharide (LPS)-induced IL-1 beta release while CQ was a more effective inhibitor of TNF-alpha production than GST. Chloroquine 103-105 tumor necrosis factor Homo sapiens 140-149 15031635-8 2003 These data demonstrate that CQ inhibits IL-1 beta release from monocytes by interfering with pretranscriptional signaling and TNF-alpha release by posttranslational events whereas GST downregulates IL-1 beta secretion by interfering with posttranslational IL-1 beta processing. Chloroquine 28-30 tumor necrosis factor Homo sapiens 126-135 11994488-1 2002 Previously, we demonstrated that the anti-inflammatory drug chloroquine (CQ) inhibited LPS-induced TNF-alpha transcription. Chloroquine 60-71 tumor necrosis factor Homo sapiens 99-108 11994488-1 2002 Previously, we demonstrated that the anti-inflammatory drug chloroquine (CQ) inhibited LPS-induced TNF-alpha transcription. Chloroquine 73-75 tumor necrosis factor Homo sapiens 99-108 11994488-4 2002 Both CQ and PD98059, a MEK1 inhibitor, reduced luciferase reporter activity driven by human TNF promoter sequences. Chloroquine 5-7 tumor necrosis factor Homo sapiens 92-95 11994488-6 2002 These findings were supported by functional data demonstrating that CQ and PD98059 interfered with TNF expression in several human and murine cell types while neither inhibitor blocked TNF production in murine RAW264.7 macrophages, a cell line that does not require MEK-ERK signaling for TNF production. Chloroquine 68-70 tumor necrosis factor Homo sapiens 99-102 9158098-3 1997 In addition, chloroquine has been shown to have inhibitory action on TNF-alpha synthesis. Chloroquine 13-24 tumor necrosis factor Homo sapiens 69-78 11849318-0 2002 Chloroquine decreases cell-surface expression of tumour necrosis factor receptors in human histiocytic U-937 cells. Chloroquine 0-11 tumor necrosis factor Homo sapiens 49-71 11849318-3 2002 We have examined the effects of anti-rheumatic drug chloroquine on the expression of cell surface and soluble TNF receptors in human histiocytic U-937 cells. Chloroquine 52-63 tumor necrosis factor Homo sapiens 110-113 11849318-4 2002 Chloroquine partially reduced production of soluble p55 and p75 TNF receptors in cells stimulated with phorbol 12-myristate 13-acetate (PMA). Chloroquine 0-11 tumor necrosis factor Homo sapiens 64-67 11849318-5 2002 In these cells, induction of both TNF receptor mRNA was not changed and the levels of cell-associated TNF receptors were rather increased by chloroquine. Chloroquine 141-152 tumor necrosis factor Homo sapiens 102-105 11849318-7 2002 Treatment of U-937 cells with chloroquine significantly reduced the level of cell surface TNF receptors and a similar effect was observed with human peripheral blood monocytes. Chloroquine 30-41 tumor necrosis factor Homo sapiens 90-93 11849318-9 2002 Our results suggest that chloroquine down-regulates cell surface TNF receptors by retarding their transport to the cell surface, while cleavage of cell surface receptors is not inhibited by chloroquine. Chloroquine 25-36 tumor necrosis factor Homo sapiens 65-68 10903761-0 2000 Chloroquine interferes with lipopolysaccharide-induced TNF-alpha gene expression by a nonlysosomotropic mechanism. Chloroquine 0-11 tumor necrosis factor Homo sapiens 55-64 10903761-2 2000 Consistent with its anti-inflammatory properties, CQ has been shown to interfere with TNF-alpha release from mononuclear phagocytes. Chloroquine 50-52 tumor necrosis factor Homo sapiens 86-95 10903761-4 2000 CQ exhibited dose-dependent inhibition of LPS-induced TNF-alpha release from human PBMC at therapeutically attainable concentrations. Chloroquine 0-2 tumor necrosis factor Homo sapiens 54-63 10903761-6 2000 CQ acted by reducing TNF-alpha mRNA accumulation without destabilizing its mRNA or interfering with NF-kappaB nuclear translocation or p50/p65 isoform composition of DNA-binding complexes. Chloroquine 0-2 tumor necrosis factor Homo sapiens 21-30 10903761-7 2000 Intracellular cytokine staining indicated that CQ reduced TNF-alpha production pretranslationally without interfering with TNF-alpha processing or release. Chloroquine 47-49 tumor necrosis factor Homo sapiens 58-67 10903761-9 2000 Although bafilomycin A1 alone did not interfere with TNF-alpha expression, preincubation augmented the ability of CQ to reduce TNF-alpha mRNA levels, suggesting that CQ did not act by a lysosomotropic mechanism. Chloroquine 114-116 tumor necrosis factor Homo sapiens 127-136 10903761-11 2000 These data indicate that CQ inhibits TNF-alpha gene expression without altering translocation of NF-kappaB p50/p65 heterodimers. Chloroquine 25-27 tumor necrosis factor Homo sapiens 37-46 9893120-13 1999 Interestingly, chloroquine also quenched the TNFalpha-induced changes in t-PA and PAI-1 mRNA levels. Chloroquine 15-26 tumor necrosis factor Homo sapiens 45-53 9893120-14 1999 Using TNFalpha mutants and agonistic or blocking monoclonal antibodies specific for the TNF receptors p55 and p75, we found evidence that chloroquine interfered with the activation of the TNF receptor p55 and/or its intracellular signaling route. Chloroquine 138-149 tumor necrosis factor Homo sapiens 6-14 9158098-5 1997 TNF-alpha and chloroquine varied in the same range on admission, but there was an inverse correlation between the two: the higher the chloroquine level, the lower the TNF-alpha level. Chloroquine 14-25 tumor necrosis factor Homo sapiens 167-176 9158098-5 1997 TNF-alpha and chloroquine varied in the same range on admission, but there was an inverse correlation between the two: the higher the chloroquine level, the lower the TNF-alpha level. Chloroquine 134-145 tumor necrosis factor Homo sapiens 0-9 9158098-8 1997 The above data suggest beneficial effects of chloroquine self-medication with respect to anti-TNF-alpha action. Chloroquine 45-56 tumor necrosis factor Homo sapiens 94-103 8357820-7 1993 Significant uptake of 125I-TNF into T-24 cells was observed when these immunoliposomes were used, and this uptake of TNF was inhibited by cytochalasin B or chloroquine. Chloroquine 156-167 tumor necrosis factor Homo sapiens 27-30 9002011-7 1997 RESULTS: We observed that chloroquine and hydroxychloroquine equally inhibit PHA induced TNF-alpha and IFN-gamma production, and LPS induced TNF-alpha and IL-6 production, while PHA induced IL-6 production was not affected. Chloroquine 26-37 tumor necrosis factor Homo sapiens 89-98 8537661-5 1996 Further, drugs such as pentoxifylline, chloroquine, and the antioxidant apocynin similarly inhibited TNF-alpha release by PG- as well as LPS-stimulated cells. Chloroquine 39-50 tumor necrosis factor Homo sapiens 101-110 9002011-0 1997 Chloroquine and hydroxychloroquine equally affect tumor necrosis factor-alpha, interleukin 6, and interferon-gamma production by peripheral blood mononuclear cells. Chloroquine 0-11 tumor necrosis factor Homo sapiens 50-77 8357820-7 1993 Significant uptake of 125I-TNF into T-24 cells was observed when these immunoliposomes were used, and this uptake of TNF was inhibited by cytochalasin B or chloroquine. Chloroquine 156-167 tumor necrosis factor Homo sapiens 117-120 34774530-6 2021 Micromolar concentrations of several DIF derivatives strongly suppressed the growth of the four laboratory strains, including strains that exhibited resistance to chloroquine and artemisinin, as well as strains that were susceptible to these drugs. Chloroquine 163-174 tumor necrosis factor Homo sapiens 37-40 8244453-0 1993 Chloroquine-induced inhibition of the production of TNF, but not of IL-6, is affected by disruption of iron metabolism. Chloroquine 0-11 tumor necrosis factor Homo sapiens 52-55 8244453-6 1993 TNF and IL-6 production were suppressed in a dose-dependent manner when macrophages were treated with chloroquine, but not with other anti-malarial drugs. Chloroquine 102-113 tumor necrosis factor Homo sapiens 0-3 8244453-8 1993 Our results demonstrated that chloroquine-induced inhibition of TNF and IL-6 production is not mediated through a lysosomotropic mechanism, and that chloroquine probably acts on TNF secretion by disrupting iron homeostasis. Chloroquine 30-41 tumor necrosis factor Homo sapiens 64-67 8244453-8 1993 Our results demonstrated that chloroquine-induced inhibition of TNF and IL-6 production is not mediated through a lysosomotropic mechanism, and that chloroquine probably acts on TNF secretion by disrupting iron homeostasis. Chloroquine 149-160 tumor necrosis factor Homo sapiens 178-181 34863979-8 2022 Knockdown of SIDT2 or pretreatment with chloroquine (a lysosome inhibitor) reduced DTX-induced NOX4 and TNF-alpha expression and mitigated JNK-mediated HuR phosphorylation. Chloroquine 40-51 tumor necrosis factor Homo sapiens 104-113 35140705-9 2021 However, the inhibition of EVR on TNF-alpha-induced EMT was partly reversed following the addition of autophagy inhibitor chloroquine. Chloroquine 122-133 tumor necrosis factor Homo sapiens 34-43