“…In cDNA microarray transcriptome analyses, we found Dlg2 highly expressed in a subpopulation of plasmacytoid DCs (pDCs) stimulated to produce type I interferons (IFNs) such as IFNβ. RESULTS: Using RACE- and RT-PCR as well as immunoprecipitation followed by Western blotting we characterised the differential expression of the Dlg2 splice variants in IFNβ-producing pDCs. …”
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“…We could previously identify RIG-I-like helicases (RLH) as targets for the immunotherapy of pancreatic cancer inducing immunogenic tumor cell death and type I interferons (IFN) as key mediators linking innate with adaptive immunity. …”
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“…Dendritic cells (DCs) release interferons (IFNs) and proinflammatory cytokines and promote adaptive immunity upon viral infection. …”
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“…The innate immune response to infection includes the release of soluble preformed mediators, or synthesis of cytoplasmic enzymes, cytokines, chemokines, interferons (IFNs), lipid mediators, proteins of the complement cascade, neurotransmitters, nucleotides, and components of transcription factors (High Mobility Group B1, receptors for sex hormones/steroids). …”
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“…Among cytokines involved in SLE pathogenesis, interferons (particularly IFN-α) and interleukin 34 play a pivotal role. …”
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“…Microglia are the primary cellular source of type I interferons (I-IFNs) in the brain upon neurotropic virus infection. …”
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“…We performed a database mining on 102 transcriptomic datasets for the expressions of 29 m(6)A-RNA methylation (epitranscriptomic) regulators (m(6)A-RMRs) in 41 diseases and cancers and made significant findings: (1) a few m(6)A-RMRs were upregulated; and most m(6)A-RMRs were downregulated in sepsis, acute respiratory distress syndrome, shock, and trauma; (2) half of 29 m(6)A-RMRs were downregulated in atherosclerosis; (3) inflammatory bowel disease and rheumatoid arthritis modulated m(6)A-RMRs more than lupus and psoriasis; (4) some organ failures shared eight upregulated m(6)A-RMRs; end-stage renal failure (ESRF) downregulated 85% of m(6)A-RMRs; (5) Middle-East respiratory syndrome coronavirus infections modulated m(6)A-RMRs the most among viral infections; (6) proinflammatory oxPAPC modulated m(6)A-RMRs more than DAMP stimulation including LPS and oxLDL; (7) upregulated m(6)A-RMRs were more than downregulated m(6)A-RMRs in cancer types; five types of cancers upregulated ≥10 m(6)A-RMRs; (8) proinflammatory M1 macrophages upregulated seven m(6)A-RMRs; (9) 86% of m(6)A-RMRs were differentially expressed in the six clusters of CD4(+)Foxp3(+) immunosuppressive Treg, and 8 out of 12 Treg signatures regulated m(6)A-RMRs; (10) immune checkpoint receptors TIM3, TIGIT, PD-L2, and CTLA4 modulated m(6)A-RMRs, and inhibition of CD40 upregulated m(6)A-RMRs; (11) cytokines and interferons modulated m(6)A-RMRs; (12) NF-κB and JAK/STAT pathways upregulated more than downregulated m(6)A-RMRs whereas TP53, PTEN, and APC did the opposite; (13) methionine-homocysteine-methyl cycle enzyme Mthfd1 downregulated more than upregulated m(6)A-RMRs; (14) m(6)A writer RBM15 and one m(6)A eraser FTO, H3K4 methyltransferase MLL1, and DNA methyltransferase, DNMT1, regulated m(6)A-RMRs; and (15) 40 out of 165 ROS regulators were modulated by m(6)A eraser FTO and two m(6)A writers METTL3 and WTAP. …”
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“…Alternatively spliced PML isoforms I-VII are expressed from one single pml gene containing nine exons and their transcription is tightly controlled and stimulated by interferons and p53. Several early HAdV proteins target PML-NBs, such as E4orf3, promoting redistribution into track-like structures. …”
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“…Interestingly, our analytical results also revealed that a cluster of differentiation 40 (CD40), plasmin, and histamine served as major regulators in the monkeypox-infected monkey MK2 cell line model, while interferons (IFNs), macrophages, and neutrophil-related signaling pathways dominated the monkeypox-infected human HeLa cell line model. …”
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“…The mRNA expression of TLR2, TLR3, TLR4, TLR9 and type I interferons (IFN) were analyzed by quantitative real-time PCR. …”
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“…Expression of type I interferons (IFNs), interleukins (IL) 5 and 10, IL-1β and granzyme B were quantified by real time PCR. …”
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“…MEDI9197 increased tumoral CD8+ and PD-L1+ cells, inducing type 1 and 2 interferons and Th1 response. There were no objective clinical responses; 10 patients in part 1 and 3 patients in part 3 had stable disease ≥8 weeks. …”
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“…Similarly, sepsis and trauma plus organ failures upregulated seven OCRG groups including vesicle, MT fission, mitophagy, sarcoplasmic reticulum–MT, MT fusion, autophagosome–lysosome fusion, and autophagosome/endosome–lysosome fusion, classified as the cell failure-handling OCRGs; (3) suppression of autophagosome–lysosome fusion in endothelial and epithelial cells is required for viral replications, which classify this decreased group as the viral replication-suppressed OCRGs; (4) pro-atherogenic damage-associated molecular patterns (DAMPs) such as oxidized low-density lipoprotein (oxLDL), lipopolysaccharide (LPS), oxidized-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (oxPAPC), and interferons (IFNs) totally upregulated 33 OCRGs in endothelial cells (ECs) including vesicle, MT fission, mitophagy, MT fusion, endoplasmic reticulum (ER)–MT contact, ER– plasma membrane (PM) junction, autophagosome/endosome–lysosome fusion, sarcoplasmic reticulum–MT, autophagosome–endosome/lysosome fusion, and ER–Golgi complex (GC) interaction as the 10 EC-activation/inflammation-promoting OCRG groups; (5) the expression of OCRGs is upregulated more than downregulated in regulatory T cells (Tregs) from the lymph nodes, spleen, peripheral blood, intestine, and brown adipose tissue in comparison with that of CD4(+)CD25(−) T effector controls; (6) toll-like receptors (TLRs), reactive oxygen species (ROS) regulator nuclear factor erythroid 2-related factor 2 (Nrf2), and inflammasome-activated regulator caspase-1 regulated the expressions of OCRGs in diseases, virus-infected cells, and pro-atherogenic DAMP-treated ECs; (7) OCRG expressions are significantly modulated in all the 28 cancer datasets, and the upregulated OCRGs are correlated with tumor immune infiltrates in some tumors; (8) tumor promoter factor IKK2 and tumor suppressor Tp53 significantly modulate the expressions of OCRGs. …”
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“…A member of the Janus kinase (JAK) family, Tyrosine Kinase 2 (TYK2), is crucial in mediating various cytokine-signaling pathways such as interleukin-23 (IL23), interleukin-12 (IL12) and type I Interferons (IFN) which contribute to autoimmune disorders (e.g., psoriasis, lupus, and inflammatory bowel disease). …”
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“…Functional cure rates are low with current treatment options (nucleos(t)ide analogs (NAs) and pegylated interferons). Bepirovirsen is an antisense oligonucleotide targeting all HBV messenger RNAs; in cell culture and animal models, bepirovirsen leads to reductions in HBV-derived RNAs, HBV DNA and viral proteins. …”
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“…Early innate immune response to HMPV is focused on induction of antiviral interferons (IFNs) and other pro-inflammatory cytokines that are critical for the formation of adaptive immune responses. …”
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“…Modest clinical benefit from type I interferons (IFN-α/β) in HAM/TSP contrasts with its recently identified IFN-inducible gene signature. …”
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“…Hydroxyurea was the most frequently used drug followed by ruxolitinib, while interferons were reported for a minority of patients. …”
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“…Dietary quercetin supplementation significantly downregulated the mRNA expression of myeloid differentiation primary response protein 88 (MyD88) and TIR domain-containing adaptor protein/MyD88-adaptor-like (TIRAP/MAL) (p < 0.05), 0.02% quercetin significantly downregulated the mRNA expression of tank-binding kinase1 (TBK1), IκB kinase complex-α (IKKα), IKKβ, IKKε, nuclear factor-kappa B (NF-κB), NF-κB inhibitor-alpha (IκBα), IκBα, IκBβ, TNF-receptor-associated factor 3 (TRAF3), and interferons regulatory factor 7 (IRF7) (p < 0.05), 0.04% quercetin significantly downregulated the mRNA expression of IKKβ, IKKε, NF-κB, IκBα, IκBβ, TRAF3, and TRAF6 (p < 0.05), and 0.06% quercetin significantly downregulated the mRNA expression of TBK1 and IKKα (p < 0.05). 0.02% quercetin significantly decreased the relative abundance of Escherichia, Staphylococcus (p < 0.05), and Salmonella (p < 0.01), 0.04% quercetin significantly decreased the relative abundance of Staphylococcus (p < 0.05), Escherichia, and Salmonella (p < 0.01), and 0.06% quercetin significantly decreased the relative abundance of Salmonella (p < 0.05) and Staphylococcus (p < 0.01) in the ileum of AA broilers. …”
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“…All patients on no DMT, interferons, glatiramer acetate, teriflunomide, natalizumab, and nearly all on fumarates had positive antibody responses post-vaccine. …”
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