PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26869429-7 2016 PolyI:C-MgPP was more efficiently taken up by toll-like receptor 3-positive RAW264.7 cells than naked polyI:C, and its uptake stimulated increased tumor necrosis factor-alpha production. Poly I-C 0-7 tumor necrosis factor Mus musculus 147-174 26772774-13 2016 Pretreating macrophages with an ERK inhibitor, U0126, dose-dependently antagonized WISP"s synergistic effect on Poly(I:C)-induced TNF-alpha release. Poly I-C 112-121 tumor necrosis factor Mus musculus 130-139 26658504-10 2015 Poly I:C also induced the expression of CXCR3 ligands, monocyte chemoattractant protein-1, IL-23p19, and TNF-alpha in the LAC in an IL-7-dependent fashion. Poly I-C 0-8 tumor necrosis factor Mus musculus 105-114 26772774-11 2016 WISP1 significantly increased Poly(I:C)-induced TNF-alpha production in macrophages isolated from WT mice but not in macrophages isolated from beta3 knock-out mice. Poly I-C 30-39 tumor necrosis factor Mus musculus 48-57 26040668-7 2015 We demonstrated that poly (I:C) induced TNFA production at a relatively high level in wild-type mice compared with that in Tlr3 knockout mice. Poly I-C 21-30 tumor necrosis factor Mus musculus 40-44 26040668-8 2015 Notably, TNFA neutralizing antibody significantly reduced poly (I:C)-induced ovarian dysfunction. Poly I-C 58-68 tumor necrosis factor Mus musculus 9-13 25840915-8 2015 Poly(I:C), but not HSV60, also dramatically induced the expression of major proinflammatory cytokines, including TNF-alpha and MCP-1, in EECs. Poly I-C 0-8 tumor necrosis factor Mus musculus 113-122 25158758-12 2014 Similarly, recombinant galectin-9 enhanced poly(I:C)-induced microglial TNF and IL-6 production. Poly I-C 43-52 tumor necrosis factor Mus musculus 72-75 24179040-4 2014 We show that pre-treatment of macrophages with Berenil dramatically suppressed IL-6, IL-12 and TNF-alpha production following LPS, CpG and Poly I:C stimulation without altering the expression of TLRs. Poly I-C 139-147 tumor necrosis factor Mus musculus 95-104 25950701-9 2015 RAG1-deficient mice given poly I:C exhibited increased frequency of TNF-alpha but not IFN-gamma/IL17A-producing ILCs in the gut and depletion of ILCs prevented the poly I:C-driven intestinal damage. Poly I-C 26-34 tumor necrosis factor Mus musculus 68-77 25950701-11 2015 Moreover, ILCs express TLR3 and are functionally able to respond to poly I:C with increased synthesis of TNF-alpha thus contributing to small intestinal atrophy. Poly I-C 68-76 tumor necrosis factor Mus musculus 105-114 24729619-11 2014 Moreover, poly(I:C) treatment attenuated the levels of TNF-alpha and IL-1beta in serum and cerebral spinal fluid of mice stimulated by LPS. Poly I-C 10-18 tumor necrosis factor Mus musculus 55-64 23640484-9 2013 In vitro studies demonstrated that KRP-203 reduced tumor necrosis factor-alpha, interleukin-6, and interferon-gamma-induced protein-10 production; IkappaB and signal transducer and activator of transcription-1 phosphorylation; and nuclear factor kappaB and signal transducer and activator of transcription-1 activation in poly(I:C)-, lipopolysaccharide-, or interferon-gamma-stimulated bone marrow macrophages, respectively. Poly I-C 322-331 tumor necrosis factor Mus musculus 51-78 23954861-6 2014 Moreover, after poly(I : C) injection, Rip3(-/-) mice displayed decreased levels of pro-inflammatory cytokines (such as TNF-alpha and IL-6) in the retina, and attenuated intravitreal release of high-mobility group box-1 (HMGB1), a major damage-associated molecular pattern (DAMP). Poly I-C 16-26 tumor necrosis factor Mus musculus 120-129 23954861-7 2014 In vitro, poly(I : C)-induced necrosis were inhibited in Rip3-deficient RPE cells, which in turn suppressed HMGB1 release and dampened TNF-alpha and IL-6 induction evoked by necrotic supernatants. Poly I-C 10-21 tumor necrosis factor Mus musculus 135-144 22983393-12 2012 Moreover, Poly I:C significantly suppressed the pro-inflammatory cytokines TNFalpha and IL-6 production. Poly I-C 10-18 tumor necrosis factor Mus musculus 75-83 23023014-9 2013 Infiltrated macrophage numbers and the expression of tumor necrosis factor-alpha, monocyte chemoattractant protein-1 and IL-6 on these cells were decreased after poly I:C treatment. Poly I-C 162-170 tumor necrosis factor Mus musculus 53-80 23028093-3 2013 Concurrently, nicotine treatment attenuated the release of IL-6 and TNF-alpha from poly(I:C)-stimulated macrophages. Poly I-C 83-92 tumor necrosis factor Mus musculus 68-77 23028093-4 2013 However, when poly(I:C)-stimulated macrophages were challenged with nicotine plus alpha-bungarotoxin (alpha-BTX), secretion of IL-6 and TNF-alpha was found to be in a level seen with poly(I:C) stimulation only, indicating that alpha7-nAChR, a highly Ca(2+) permeable ion channel sensitive to blockade by alpha-BTX, is involved in this process. Poly I-C 14-23 tumor necrosis factor Mus musculus 136-145 23028093-4 2013 However, when poly(I:C)-stimulated macrophages were challenged with nicotine plus alpha-bungarotoxin (alpha-BTX), secretion of IL-6 and TNF-alpha was found to be in a level seen with poly(I:C) stimulation only, indicating that alpha7-nAChR, a highly Ca(2+) permeable ion channel sensitive to blockade by alpha-BTX, is involved in this process. Poly I-C 14-22 tumor necrosis factor Mus musculus 136-145 22809727-8 2012 Moreover, FN reduced TNF-alpha production induced by polyI:C (TLR3 ligand), and imiquimod (TLR7 ligand), but not by LPS (TLR4 ligand), or a non-CpG pDNA/cationic liposome complex. Poly I-C 53-60 tumor necrosis factor Mus musculus 21-30 22581266-13 2012 Poly (I:C)-induced TNF-alpha, and IL-6 in vitro demonstrated no difference between GS/GS mice and WT mice. Poly I-C 0-10 tumor necrosis factor Mus musculus 19-28 22765163-6 2012 RESULTS: TNF-alpha production was enhanced by airway exposure to low and high doses of poly[I:C]. Poly I-C 87-95 tumor necrosis factor Mus musculus 9-18 22765163-10 2012 Moreover, the Th2 cell response induced by sensitization with OVA plus low-dose poly[I:C], which was abolished in TNF-alpha-deficient mice, was restored in these mice upon addition of recombinant TNF-alpha. Poly I-C 80-88 tumor necrosis factor Mus musculus 114-123 22765163-10 2012 Moreover, the Th2 cell response induced by sensitization with OVA plus low-dose poly[I:C], which was abolished in TNF-alpha-deficient mice, was restored in these mice upon addition of recombinant TNF-alpha. Poly I-C 80-88 tumor necrosis factor Mus musculus 196-205 22308357-6 2012 TNF-alpha was increased within 1 h in both tumor and serum upon polyI:C injection into tumor-bearing mice, followed by tumor hemorrhagic necrosis and growth suppression. Poly I-C 64-71 tumor necrosis factor Mus musculus 0-9 22361747-5 2012 Poly(I:C)-stimulated NOD.Ncf1(m1J) BM-Mphi exhibited a 2- and 10-fold decrease in TNF-alpha and IFN-beta proinflammatory cytokine synthesis, respectively, in contrast to NOD BM-Mphi. Poly I-C 0-9 tumor necrosis factor Mus musculus 82-91 22308357-8 2012 Furthermore, F4/80(+) Mfs in tumors extracted from polyI:C-injected mice sustained Lewis lung carcinoma cytotoxic activity, and this activity was partly abrogated by anti-TNF-alpha Ab. Poly I-C 51-58 tumor necrosis factor Mus musculus 171-180 16831928-10 2006 To demonstrate this, we injected wild-type C57B/6 and TNF-Tg mice with poly I:C, which is known to induce systemic IFN responses, and show its dominant effects on increasing the number of circulating CD11b+/CD11c+ precursor dendritic cells (pDC), concomitant with a dramatic reduction in CD11b+/CD11c- OCP. Poly I-C 71-79 tumor necrosis factor Mus musculus 54-57 21206981-5 2011 When stimulated with poly I:C (and also LPS) JAWSII cells produced large amounts of IL-6, TNF-alpha and MCP-1. Poly I-C 21-29 tumor necrosis factor Mus musculus 90-99 20218969-3 2010 Results showed that exogenously added apoE suppressed the LPS and poly(I-C) induction of IL (interleukin)-6, IL-1beta and TNF-alpha (tumour necrosis factor-alpha) secretion by RAW 264.7 cells. Poly I-C 66-75 tumor necrosis factor Mus musculus 122-131 19036857-3 2009 Whereas extracellular poly I:C (naked poly I:C) mainly induced the expression of regulated on activation normal T-cell expressed and secreted (RANTES), interleukin-8 (IL-8), and tumor necrosis factor alpha (TNF-alpha), intracellular delivery of poly I:C (complexed poly I:C) chiefly induced expression of IFN-beta and IL-6. Poly I-C 22-30 tumor necrosis factor Mus musculus 178-205 19036857-3 2009 Whereas extracellular poly I:C (naked poly I:C) mainly induced the expression of regulated on activation normal T-cell expressed and secreted (RANTES), interleukin-8 (IL-8), and tumor necrosis factor alpha (TNF-alpha), intracellular delivery of poly I:C (complexed poly I:C) chiefly induced expression of IFN-beta and IL-6. Poly I-C 22-30 tumor necrosis factor Mus musculus 207-216 19036857-3 2009 Whereas extracellular poly I:C (naked poly I:C) mainly induced the expression of regulated on activation normal T-cell expressed and secreted (RANTES), interleukin-8 (IL-8), and tumor necrosis factor alpha (TNF-alpha), intracellular delivery of poly I:C (complexed poly I:C) chiefly induced expression of IFN-beta and IL-6. Poly I-C 38-46 tumor necrosis factor Mus musculus 178-205 19036857-3 2009 Whereas extracellular poly I:C (naked poly I:C) mainly induced the expression of regulated on activation normal T-cell expressed and secreted (RANTES), interleukin-8 (IL-8), and tumor necrosis factor alpha (TNF-alpha), intracellular delivery of poly I:C (complexed poly I:C) chiefly induced expression of IFN-beta and IL-6. Poly I-C 38-46 tumor necrosis factor Mus musculus 207-216 19036857-3 2009 Whereas extracellular poly I:C (naked poly I:C) mainly induced the expression of regulated on activation normal T-cell expressed and secreted (RANTES), interleukin-8 (IL-8), and tumor necrosis factor alpha (TNF-alpha), intracellular delivery of poly I:C (complexed poly I:C) chiefly induced expression of IFN-beta and IL-6. Poly I-C 38-46 tumor necrosis factor Mus musculus 178-205 19036857-3 2009 Whereas extracellular poly I:C (naked poly I:C) mainly induced the expression of regulated on activation normal T-cell expressed and secreted (RANTES), interleukin-8 (IL-8), and tumor necrosis factor alpha (TNF-alpha), intracellular delivery of poly I:C (complexed poly I:C) chiefly induced expression of IFN-beta and IL-6. Poly I-C 38-46 tumor necrosis factor Mus musculus 207-216 19036857-3 2009 Whereas extracellular poly I:C (naked poly I:C) mainly induced the expression of regulated on activation normal T-cell expressed and secreted (RANTES), interleukin-8 (IL-8), and tumor necrosis factor alpha (TNF-alpha), intracellular delivery of poly I:C (complexed poly I:C) chiefly induced expression of IFN-beta and IL-6. Poly I-C 38-46 tumor necrosis factor Mus musculus 178-205 19036857-3 2009 Whereas extracellular poly I:C (naked poly I:C) mainly induced the expression of regulated on activation normal T-cell expressed and secreted (RANTES), interleukin-8 (IL-8), and tumor necrosis factor alpha (TNF-alpha), intracellular delivery of poly I:C (complexed poly I:C) chiefly induced expression of IFN-beta and IL-6. Poly I-C 38-46 tumor necrosis factor Mus musculus 207-216 17877757-6 2007 The inhibitory effects of AICAR in poly (I:C)-mediated signalling for NF-kappaB activation and production of TNF-alpha were analysed in vitro. Poly I-C 35-45 tumor necrosis factor Mus musculus 109-118 17877757-8 2007 Interestingly, AICAR significantly attenuated poly (I:C)-induced airway hyperresponsiveness and airway inflammation, as shown by the attenuation of the influx of total inflammatory cells and soluble products into bronchoalveolar lavage fluid, such as macrophages, eosinophils, IL-5, IL-13, TNF-alpha and IFN-gamma. Poly I-C 46-56 tumor necrosis factor Mus musculus 290-299 17877757-11 2007 Moreover, AICAR effectively inhibited poly (I:C)-mediated activation of NF-kappaB and the production of TNF-alpha. Poly I-C 38-48 tumor necrosis factor Mus musculus 104-113 17196665-7 2007 Meanwhile, 24h after poly I:C injection, expression of TLR3 was markedly elevated within decidua basalis (DB), and endometrial TNF-alpha increased 2.7-fold but IFN-gamma remained unchanged in homogenized endometrium. Poly I-C 21-29 tumor necrosis factor Mus musculus 127-136 17267173-3 2007 In naive mice, poly I:C (2mg/kg) modestly increased sickness behaviors, plasma IL-6, TNF-alpha and IL-10 levels, but did not affect IL-1, IL-4, or IFN-gamma. Poly I-C 15-23 tumor necrosis factor Mus musculus 85-94 21111765-8 2011 Importantly, whereas injection of soluble poly(I:C) led to rapid production of the pro-inflammatory cytokines tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 in serum, administration of poly(I:C) in complex with the cationic DDA/TDB liposomes prevented this non-specific systemic pro-inflammatory response. Poly I-C 42-50 tumor necrosis factor Mus musculus 110-143 21111765-8 2011 Importantly, whereas injection of soluble poly(I:C) led to rapid production of the pro-inflammatory cytokines tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 in serum, administration of poly(I:C) in complex with the cationic DDA/TDB liposomes prevented this non-specific systemic pro-inflammatory response. Poly I-C 195-203 tumor necrosis factor Mus musculus 110-143 20448144-6 2010 Poly I:C and CCl(4) cotreatment synergistically induced accumulation of NK cells in the liver and NK cell production of IFN-gamma and tumor necrosis factor (TNF)-alpha. Poly I-C 0-8 tumor necrosis factor Mus musculus 134-167 20448144-8 2010 Finally, blockage of TNF-alpha but not IFN-gamma restored liver regeneration in poly I:C/CCl(4)-treated mice. Poly I-C 80-88 tumor necrosis factor Mus musculus 21-30 20448144-9 2010 Taken together, these findings suggest that poly I:C treatment inhibits liver regeneration in the CCl(4)-induced liver injury model via induction of NK cell production of TNF-alpha. Poly I-C 44-52 tumor necrosis factor Mus musculus 171-180 19111017-7 2009 Posttreatment with polyI:C also caused activation of hepatic Kupffer cells (KCs) and natural killer (NK) cells and upregulated multiple proapoptotic factors, including tumor necrosis factor-alpha (TNF-alpha), NK receptor group 2, member D (NKG2D), and Fas ligand (FasL). Poly I-C 19-26 tumor necrosis factor Mus musculus 168-195 19111017-7 2009 Posttreatment with polyI:C also caused activation of hepatic Kupffer cells (KCs) and natural killer (NK) cells and upregulated multiple proapoptotic factors, including tumor necrosis factor-alpha (TNF-alpha), NK receptor group 2, member D (NKG2D), and Fas ligand (FasL). Poly I-C 19-26 tumor necrosis factor Mus musculus 197-206 18809435-9 2008 Both mAbs to SHPS-1, but not that to CD47, also inhibited the lipopolysaccharide- or polyinosinic-polycytidylic acid-induced production of TNF-alpha by DCs. Poly I-C 85-116 tumor necrosis factor Mus musculus 139-148 18331798-4 2008 We report that also polyinosinic-polycytidylic acid [poly(I:C)], a TLR-3 agonist, induces systemic TNF in mice. Poly I-C 20-51 tumor necrosis factor Mus musculus 99-102 18331798-4 2008 We report that also polyinosinic-polycytidylic acid [poly(I:C)], a TLR-3 agonist, induces systemic TNF in mice. Poly I-C 53-62 tumor necrosis factor Mus musculus 99-102 18331798-6 2008 Our results provide direct evidence that poly(I:C) induces TNF-alpha in d-GalN sensitized mice, which leads to severe, acute, and TNF-dependent lethal hepatitis. Poly I-C 41-50 tumor necrosis factor Mus musculus 59-68 18331798-6 2008 Our results provide direct evidence that poly(I:C) induces TNF-alpha in d-GalN sensitized mice, which leads to severe, acute, and TNF-dependent lethal hepatitis. Poly I-C 41-50 tumor necrosis factor Mus musculus 59-62 17072335-5 2007 Analysis of the innate immune response in the DNA-PKcs-deficient mice with short dysfunctional telomeres revealed high basal serum levels of tumor necrosis factor alpha (TNFalpha) and hyper-active cytokine responses upon challenge with polyinosinic-polycytidylic acid (poly-IC). Poly I-C 236-267 tumor necrosis factor Mus musculus 141-168 11269746-3 2001 We have combined in the present study the NK-enhancing properties of IFN (Poly I:C-induced) and TNF-alpha by giving Poly I:C to leukemic mice for 8 days after irradiation and SBMT, concomitant with TNF-alpha during the first 4 days immediately after SBMT. Poly I-C 74-82 tumor necrosis factor Mus musculus 198-207 16265667-4 2006 Our results show that the injection of polyinosinic-polycytidylic acid (poly(I:C)), a synthetic dsRNA, into the striatum of the mouse brain induces the activation of astrocytes and the expression of TNF-alpha, IFN-beta, and IP-10. Poly I-C 39-70 tumor necrosis factor Mus musculus 199-208 16265667-4 2006 Our results show that the injection of polyinosinic-polycytidylic acid (poly(I:C)), a synthetic dsRNA, into the striatum of the mouse brain induces the activation of astrocytes and the expression of TNF-alpha, IFN-beta, and IP-10. Poly I-C 72-81 tumor necrosis factor Mus musculus 199-208 11269746-6 2001 RESULTS: The data reveal that TNF-alpha, added to the Poly I:C administration protocol, significantly boosted NK cell numbers 2.4-fold over that achieved by Poly I:C alone. Poly I-C 54-62 tumor necrosis factor Mus musculus 30-39 11269746-6 2001 RESULTS: The data reveal that TNF-alpha, added to the Poly I:C administration protocol, significantly boosted NK cell numbers 2.4-fold over that achieved by Poly I:C alone. Poly I-C 157-165 tumor necrosis factor Mus musculus 30-39 1839310-2 1991 The poly(I:C)-induced intratumor hemorrhagic reaction was associated with production of appreciable quantities of tumor necrosis factor (TNF) by the host. Poly I-C 4-13 tumor necrosis factor Mus musculus 114-135 1839310-2 1991 The poly(I:C)-induced intratumor hemorrhagic reaction was associated with production of appreciable quantities of tumor necrosis factor (TNF) by the host. Poly I-C 4-13 tumor necrosis factor Mus musculus 137-140 34454033-5 2022 Maoto significantly decreased PolyI:C-induced TNF-alpha levels and increased IL-10 production. Poly I-C 30-37 tumor necrosis factor Mus musculus 46-55 2111350-5 1990 Hence, Poly I:C-induced macrophage-mediated cytolysis of 3LL-R cells may result from 1) the induction of macrophages by Poly I:C to secrete high amounts of TNF-alpha and class I IFN and 2) a synergism between IFN-alpha/IFN-beta and TNF-alpha on lysis of 3LL-R cells. Poly I-C 7-15 tumor necrosis factor Mus musculus 156-165 2111350-5 1990 Hence, Poly I:C-induced macrophage-mediated cytolysis of 3LL-R cells may result from 1) the induction of macrophages by Poly I:C to secrete high amounts of TNF-alpha and class I IFN and 2) a synergism between IFN-alpha/IFN-beta and TNF-alpha on lysis of 3LL-R cells. Poly I-C 7-15 tumor necrosis factor Mus musculus 232-241 2111350-5 1990 Hence, Poly I:C-induced macrophage-mediated cytolysis of 3LL-R cells may result from 1) the induction of macrophages by Poly I:C to secrete high amounts of TNF-alpha and class I IFN and 2) a synergism between IFN-alpha/IFN-beta and TNF-alpha on lysis of 3LL-R cells. Poly I-C 120-128 tumor necrosis factor Mus musculus 156-165 2111350-0 1990 Poly I:C activated macrophages are tumoricidal for TNF-alpha-resistant 3LL tumor cells. Poly I-C 0-8 tumor necrosis factor Mus musculus 51-60 34454033-7 2022 Furthermore, the inhibitory effects of maoto on PolyI:C-induced TNF-alpha production were not observed in ex vivo splenocytes, suggesting that maoto does not act directly on inflammatory cells. Poly I-C 48-55 tumor necrosis factor Mus musculus 64-73 34903784-6 2021 We find that, 4 h after the administration, both poly I:C and resiquimod elevated the levels of IL-6, TNFalpha, and chemokines including CCL2 and CCL5, in maternal plasma. Poly I-C 49-57 tumor necrosis factor Mus musculus 102-110 34903784-8 2021 In foetal brain, poly I:C produced no detectable immune-response-related increases, whereas pronounced increases in cytokine (e.g. Il-6, Tnfalpha) and chemokine (e.g. Ccl2, Ccl5) expression were observed with maternal resiquimod administration. Poly I-C 17-25 tumor necrosis factor Mus musculus 137-145 34665110-8 2021 Further, polyI:C stimulation of bone marrow-derived macrophages (BMDMs) induced TNF-alpha, IFN-beta, IL-6 and Nos-2, but responses were not different in BMDMs generated from WT or vip-/- mice. Poly I-C 9-16 tumor necrosis factor Mus musculus 80-89 34453520-6 2021 Poly(I:C) dramatically induced the expression of the pro-inflammatory cytokines TNF-alpha and IL-6 in SC and LC through Toll-like receptor 3 and IFN-beta promoter stimulator 1 signaling pathways, impairing the integrity of the blood-testis barrier and testosterone synthesis. Poly I-C 0-9 tumor necrosis factor Mus musculus 80-89 34453520-7 2021 Poly(I:C)-induced TNF-alpha production thus plays a critical role in the impairment of cell functions. Poly I-C 0-9 tumor necrosis factor Mus musculus 18-27 3447151-9 1987 It was of interest that coincubating poly(I,C)-LC and peritoneal macrophages in vitro resulted in the production of tumor necrosis factor, which has a similar pattern of toxicity; this finding suggests that poly(I,C)-LC"s pattern of toxicity may be associated with the induction of TNF and/or IFN. Poly I-C 37-45 tumor necrosis factor Mus musculus 282-285 3447151-9 1987 It was of interest that coincubating poly(I,C)-LC and peritoneal macrophages in vitro resulted in the production of tumor necrosis factor, which has a similar pattern of toxicity; this finding suggests that poly(I,C)-LC"s pattern of toxicity may be associated with the induction of TNF and/or IFN. Poly I-C 37-46 tumor necrosis factor Mus musculus 282-285 32390869-5 2020 In response to poly(I:C) stimulation, PKCdelta deficient macrophages displayed an increased production of IL-1beta, IL-6, TNF-alpha, and IL-33, which were associated with an enhanced NF-kappaB activation. Poly I-C 15-24 tumor necrosis factor Mus musculus 122-131 33892139-6 2021 High molecular weight (HMW) poly I:C (1-6kb, 12 mg/kg) produced more robust sickness behavior and more robust IL-6, IFN-I and TNF-alpha responses than poly I:C of <500 bases (low MW) preparations. Poly I-C 28-36 tumor necrosis factor Mus musculus 126-135 33442686-6 2021 High molecular weight (HMW) poly I:C (1 to 6 kb, 12 mg/kg) produced more robust sickness behavior and more robust IL-6, IFN-I and TNF alpha responses than poly I:C of less than 500 bases (low MW) preparations. Poly I-C 28-36 tumor necrosis factor Mus musculus 130-139 34028652-7 2021 Polyinosinic: polycytidylic acid (poly [I:C])-stimulated macrophage cells and 10-7 M 1,25 OH-vitamin D3 significantly decreased gene expression of ICAM1, TLR3, IL6, IL8, and TNFalpha (P < 0.0001). Poly I-C 34-44 tumor necrosis factor Mus musculus 174-182 33383149-11 2021 In conclusion, the exogenous IL-33 administration mitigated liver injury and inflammation (decreased levels of IFNgamma and TNFalpha) in Poly I:C and ConA-induced acute hepatitis in mice. Poly I-C 137-145 tumor necrosis factor Mus musculus 124-132 32328062-7 2020 The oral administration of L. plantarum WT to mice prior the intraperitoneal injection of poly(I:C) significantly increased IFN-beta and IL-10 and reduced intraepithelial lymphocytes (CD3+NK1.1+CD8alphaalpha+) and pro-inflammatory mediators (TNF-alpha, IL-6, and IL-15) in the intestinal mucosa. Poly I-C 90-99 tumor necrosis factor Mus musculus 242-251 32328942-3 2020 In 3 h after combined addition of LPS and Poly I:C in vitro to 12-day-old primary culture of mouse bone marrow stromal cells, the concentration of TNFalpha in culture medium was intermediate between the levels attained by their individual application. Poly I-C 42-50 tumor necrosis factor Mus musculus 147-155 32322251-5 2020 Orally administered MPL16 prior intraperitoneal injection of poly(I:C) significantly reduced the levels of the proinflammatory mediators tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), and IL-15 in the intestinal mucosa. Poly I-C 61-70 tumor necrosis factor Mus musculus 166-175 28747347-4 2017 TRIM8 deficiency leads to increased polyinosinic-polycytidylic acid- and LPS-triggered induction of downstream anti-microbial genes including TNF, Il6, Rantes, and Ifnb, evaluated serum cytokine levels, and increased susceptibility of mice to polyinosinic-polycytidylic acid- and LPS-induced inflammatory death as well as Salmonella typhimurium infection-induced loss of body weight and septic shock. Poly I-C 36-67 tumor necrosis factor Mus musculus 142-145 31500303-5 2019 Wild type (WT) mice treated with poly(I:C) exhibited altered expression patterns of TNF and IL-12p40 during CASP which were dependent on IFNbeta or IFNAR1, suggesting a mechanism for the increased sepsis susceptibility of WT mice. Poly I-C 33-42 tumor necrosis factor Mus musculus 84-87 31057355-6 2019 Poly(I:C) increased the circulating levels of cytokines (TNF-alpha, MCP-1, IL-6, IL-10, IFN-alpha, IFN-gamma), an effect amplified by IF. Poly I-C 0-8 tumor necrosis factor Mus musculus 57-66 30613299-10 2018 However, FMT combined with PIC synergistically inhibited their proliferation by shifting macrophages to a tumoricidal phenotype with upregulated TNF-alpha and iNOS, increased NO secretion and augmented phagocytosis induced by NOX2-derived ROS in vitro. Poly I-C 27-30 tumor necrosis factor Mus musculus 145-154 28958936-6 2017 M8I inhibited the LPS- or poly(I:C)-induced production of the tumor necrosis factor-alpha and nitric oxide, alone or in combination with CSF-1 or IL-34. Poly I-C 26-35 tumor necrosis factor Mus musculus 62-89 27311810-0 2016 Polyinosinic-polycytidylic acid inhibits the differentiation of mouse preadipocytes through pattern recognition receptor-mediated secretion of tumor necrosis factor-alpha. Poly I-C 0-31 tumor necrosis factor Mus musculus 143-170 27311810-10 2016 The effect of poly(I:C) stimulation, either through endogenous transfection or exogenous addition, on inhibition of differentiation was significantly diminished in the preadipocytes of TNF-alpha knockout mice. Poly I-C 14-23 tumor necrosis factor Mus musculus 185-194 27311810-11 2016 These results confirmed the evidence that poly(I:C) inhibited the differentiation of mouse preadipocytes through PRR-mediated secretion of TNF-alpha. Poly I-C 42-51 tumor necrosis factor Mus musculus 139-148 28246473-11 2017 By contrast, poly I:C pretreatment markedly reversed the DSS-induced up-regulated expressions of the inflammatory cytokines TNF-alpha, IL-17 and IFN-gamma. Poly I-C 13-21 tumor necrosis factor Mus musculus 124-133 27614570-6 2016 PolyI:C treatment of murine microglial cells activated the production of TNF-alpha and enhanced the p38 mitogen-activated protein kinase (MAPK) pathway, whereas aripiprazole inhibited these responses. Poly I-C 0-7 tumor necrosis factor Mus musculus 73-82