JCI - Gout: new insights into an old disease
A key structural motif involved in TLR signaling is the Toll/IL-1 receptor (TIR) domain. TIR can be found in the cytoplasmic portion of all TLRs, members of the IL-1 receptor (IL-1R) family, and a group of adaptor proteins including myeloid differentiation primary response protein 88 (MyD88), TIR domain-containing adaptor protein (TIRAP), TIR domain-containing adaptor-inducing IFN-β (TRIF), and TRIF-related adaptor molecule (TRAM), all of which play fundamental roles in TLR and IL-1R signaling (9). When Chen et al. analyzed mice deficient in these adaptors, MSU crystal-induced inflammation was not impaired in TIRAP-, TRIF-, and TRAM-deficient mice but, surprisingly, was almost completely abolished by MyD88 deficiency (7). This prompted the authors to investigate the role of the IL-1Rs, the other receptor family that signals via MyD88, and led to the provocative observation that MSU ...https://www.jci.org/articles/view/JCI29404
Toll-like receptor-2 mediates inflammation and matrix degradation in human atherosclerosis. - The Kennedy Institute of...
BACKGROUND: Inflammation and matrix degradation are the hallmarks of high-risk atherosclerosis that leads to myocardial infarction and stroke. Toll-like receptors (TLRs), key players in innate immunity, are upregulated in atherosclerotic lesions, but their functional role in human atherosclerosis is unknown. We explored the effects of blocking TLR-2, TLR-4, and myeloid differentiation primary response gene 88 (MyD88), a signaling adaptor shared by most TLRs and interleukin-1 receptor (IL-1R), in an in vitro model of human atherosclerosis. METHODS AND RESULTS: Carotid endarterectomies were obtained from patients with symptomatic carotid disease. Cells were isolated via enzymatic tissue dissociation and cultured in the presence or absence of TLR signaling blockers. A dominant-negative form of MyD88 (MyD88(DN)) decreased the production of monocyte chemotactic protein-1/CCL2 (P=0.000), IL-8/CXCL8 (P=0.006), IL-6 (P=0.002), matrix metalloproteinase-1 (MMP-1; ...https://www.kennedy.ox.ac.uk/publications/224454
OriGene - MYD88 (NM 001172566) cDNA Clone
MYD88 - MYD88 (untagged)-Human myeloid differentiation primary response gene (88) (MYD88) transcript variant 5 available for purchase from OriGene - Your Gene Company.http://www.origene.com/cdna/trueclone/accession/NM_001172566/SC328250.aspx
MyD88-dependent toll-like receptor signalling is not a requirement for fetal islet xenograft rejection in mice
BACKGROUND: Rejection of pancreatic islet xenografts in mice shares immunopathological features with a Th1-associated delayed-type hypersensitivity (DTH) reaction. The aim of the present study was to investigate the mechanism of acute cellular xenograft rejection in a strain of mice with a targeted gene disruption of the toll-like receptor (TLR) signal adaptor protein MyD88. These mice have been shown to have markedly impaired Th1 immunity.. METHODS: The MyD88-/- and normal mice were transplanted with 2 microl of fetal porcine islet-like cell clusters (ICC) under the left kidney capsule. On days 3, 6 or 12 after transplantation the mice were killed and the grafts either prepared for immunohistochemistry or real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR). The number of remaining ICC and infiltrating cells with different phenotypic characteristics was assessed semi-quantitatively. Grafts used for quantitative RT-PCR were analysed for content of murine mRNA of ...http://uu.diva-portal.org/smash/record.jsf?pid=diva2:53488
Innate Immunity | Williams Hematology, 9e | AccessHemOnc | McGraw-Hill Medical
Acronyms and Abbreviations BIR, baculovirus inhibitor of apoptosis repeat; CARD, caspase activating and recruitment domain; CD, cluster of differentiation; cGAS, cyclic AMP/GMP synthetase; CTLA, cytotoxic T-lymphocyte antigen; DAI, DNA-dependent activator of IRFs; ERK, extracellular signal-regulated kinase; FADD, Fas-associated death domain; G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte-monocyte colony-stimulating factor; IFN, interferon; IκB; inhibitor of κB; IKK, IκB kinase; IL, interleukin; IPAF, ice-protease activating factor; IPS-1, IFN-β promoter stimulator 1; IRAK, interleukin-1 receptor-associated kinase; IRF, interferon response factor; JAK, Janus kinase; JNK, c-Jun N-terminal kinase; LPS, lipopolysaccharide; LRR, leucine-rich repeat; MAL, MyD88 adaptor-like; MDA5, melanoma differentiation-associated gene 5; MDP, muramyl dipeptide; MyD88, myeloid ...http://hemonc.mhmedical.com/content.aspx?bookid=1581§ionid=108043306
Most recent papers with the keyword Interferon-induced depression | Read by QxMD
This study aimed to investigate the effects of choline deficiency on intestinal inflammation of fish after Aeromonas hydrophila infection and the potential molecular mechanisms. Juvenile Jian carp (Cyprinus carpio var. Jian) were fed two diets containing choline at 165 (deficient group) and 607 mg/kg diet respectively for 65 days. Choline deficiency decreased intestinal lysozyme activity, C3 and IgM contents, increased acid phosphatase activity, downregulated mRNA levels of antimicrobial peptides [liver-expressed antimicrobial peptide (LEAP) 2A, LEAP-2B, hepcidin and defensin], cytokines [interleukin (IL) 6a, tumor necrosis factor α (TNF-α), interferon γ2b (IFN-γ2b), IL-6b and transforming growth factor β2 (TGF-β2) only in proximal intestine, IL-10 in mid and distal intestine], immune-related signaling molecules [Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), nuclear factor kappa B (NF-κB), ...https://www.readbyqxmd.com/keyword/95557
Plasmodium berghei Infection in Mice Induces Liver Injury by an IL-12- and Toll-Like Receptor/Myeloid Differentiation Factor 88...
The cytokines IL-12 and IL-18 can play a critical role in the induction of liver injury following infection. In a previous study, we showed that sequential administration of heat-killed Propionibacterium acnes, a Gram-positive bacterium, and LPS induces acute liver injury in mice (13, 36). In this model, P. acnes-elicited Kupffer cells produce IL-12 and IL-18 in response to LPS challenge which results in induction of hepatotoxic TNF-α and Fas L in the liver (28, 36). Liver injury in this model is prevented by the administration of neutralizing anti-IL-18 Abs (13) and is absent in IL-18-deficient mice (37), indicating that IL-18 is essential for P. acnes and LPS-induced liver injury. Furthermore, liver injury in this model was dependent on induction of Fas L expression but independent of perforin (11). Thus, IL-18 is required for the induction of some types of liver injury. In contrast, the studies described demonstrate that P. berghei-induced liver injury is independent of IL-18 but dependent ...http://www.jimmunol.org/content/167/10/5928.long
Human Cytomegalovirus-Platelet Interaction Triggers Toll-Like Receptor 2-Dependent Proinflammatory and Proangiogenic...
HCMV is released into the blood during active infection, allowing HCMV-platelet interactions. Here, for the first time, we show that HCMV predominately bound to a TLR2-positive platelet subpopulation, leading to the induction of platelet activation through a TLR2-dependent pathway. Platelet activation by HCMV could be completely abolished on blocking TLR2 receptor or inhibition of phosphoinositide 3-kinase signaling, which is a key mediator in TLR2-induced platelet activation.19 Platelets have been reported previously to express TLR2 on the surface of 4% to 16% platelets.14-16 However, in our study, these levels were lower with 1.3% to 3% TLR2-positive platelets, which strongly correlated with the percentage of HCMV-bound platelets. Despite the low percentage of TLR2-positive platelets, ≈20% of platelets became P-selectin positive in response to HCMV, indicating that activation of the TLR2-positive subpopulation triggered further platelet activation in a TLR2-independent fashion. This ...http://atvb.ahajournals.org/content/34/4/801
TLR Signals Promote IL-6/IL-17-Dependent Transplant Rejection | The Journal of Immunology
We have previously shown that TLR signals at the time of transplantation can prevent cardiac allograft acceptance normally induced by anti-CD154. Our current results demonstrate that this TLR-induced rejection depends on the combination of IL-6 and IL-17 signals. In addition, blockade of IL-6 and IL-17 does not prevent cardiac allograft rejection in nonimmunosuppressed recipients that did not receive CpG, indicating that TLR signals at the time of transplantation trigger acute rejection in anti-CD154-treated recipients by a mechanism distinct from that in untreated controls.. Our data show that the pro-rejection effect of CpG depends on recipient hemopoietic cells and that administration of CpG results in the rapid systemic production of IL-12 and IL-6 and the subsequent expression of IFN-γ and IL-17 by graft-infiltrating CD4+ T cells despite anti-CD154 treatment. These observations suggest a model in which TLR signals activate host innate immune cells resulting in Th1 and Th17 ...http://www.jimmunol.org/content/182/10/6217.long
Biological Process: apoptosis; cell activation; cytokine secretion involved in immune response; defense response to Gram-positive bacterium; detection of diacyl bacterial lipopeptide; detection of triacylated bacterial lipoprotein; I-kappaB phosphorylation; immune response; inflammatory response; innate immune response; interleukin-10 production; learning; leukotriene metabolic process; lipopolysaccharide-mediated signaling pathway; microglia development; microglial cell activation; MyD88-dependent toll-like receptor signaling pathway; myelin formation in the central nervous system; negative regulation of cell proliferation; negative regulation of phagocytosis; negative regulation of synaptogenesis; neutrophil degranulation; nitric oxide metabolic process; positive regulation of chemokine production; positive regulation of inflammatory response; positive regulation of interferon-beta production; positive regulation of interleukin-10 production; positive regulation of interleukin-12 production; ...https://www.phosphosite.org/proteinAction.action?id=20211
MyD88-dependent TLR signals are necessary and sufficient to confer dendritic cells with gut-specific imprinting properties. ...
Lymphocyte migration is at the heart of normal and pathological immune responses in the intestinal mucosa. We and others have shown that, in addition to activating lymphocytes, gut-associated dendritic cells (GALT-DC) can metabolize dietary vitamin A into all-trans retinoic acid (RA), which is required for inducing gut-tropic lymphocytes and IgA antibody-secreting cells (IgA-ASC). GALT-DC from mice deficient in the intracellular signaling adaptor MyD88, which lack most Toll-like receptor (TLR) signals, were significantly impaired in their capacity to induce gut-homing T cells and IgA-ASC and expressed low levels of retinal dehydrogenases (RALDH), which are critical enzymes for RA biosynthesis. MyD88-/- mice were also impaired in generating gut-tropic T cells upon immunization and exhibited low numbers of intestinal IgA-ASC. Pre-treatment of murine spleen-DC and human monocyte-derived DC with a TLR1/2 agonist was sufficient to induce RALDH and to confer these extra-intestinal DC with the ...http://www.jimmunol.org/content/186/1_Supplement/161.2
IJERPH | Free Full-Text | SNP-SNP Interaction between TLR4 and MyD88 in Susceptibility to Coronary Artery Disease in the...
The toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-dependent signaling pathway plays a role in the initiation and progression of coronary artery disease (CAD). We investigated SNP-SNP interactions between the TLR4 and MyD88 genes in CAD susceptibility and assessed whether the effects of such interactions were modified by confounding risk factors (hyperglycemia, hyperlipidemia and Helicobacter pylori (H. pylori) infection). Participants with CAD (n = 424) and controls (n = 424) without CAD were enrolled. Polymerase chain restriction-restriction fragment length polymorphism was performed on genomic DNA to detect polymorphisms in TLR4 (rs10116253, rs10983755, and rs11536889) and MyD88 (rs7744). H. pylori infections were evaluated by enzyme-linked immunosorbent assays, and the cardiovascular risk factors for each subject were evaluated clinically. The significant interaction between TLR4 rs11536889 and ...http://www.mdpi.com/1660-4601/13/3/278
"Specific inhibition of MyD88-independent signaling pathways of TLR3 an" by Hyung S. Youn, Joo Y. Lee et al.
TLRs can activate two distinct branches of downstream signaling pathways. MyD88 and Toll/IL-1R domain-containing adaptor inducing IFN-beta (TRIF) pathways lead to the expression of proinflammatory cytokines and type I IFN genes, respectively. Numerous reports have demonstrated that resveratrol, a phytoalexin with anti-inflammatory effects, inhibits NF-kappaB activation and other downstream signaling pathways leading to the suppression of target gene expression. However, the direct targets of resveratrol have not been identified. In this study, we attempted to identify the molecular target for resveratrol in TLR-mediated signaling pathways. Resveratrol suppressed NF-kappaB activation and cyclooxygenase-2 expression in RAW264.7 cells following TLR3 and TLR4 stimulation, but not TLR2 or TLR9. Further, resveratrol inhibited NF-kappaB activation induced by TRIF, but not by MyD88. The activation of IFN regulatory factor 3 and the expression of IFN-beta induced by LPS, poly(I:C), ...http://escholarship.umassmed.edu/infdis_pp/87/
TICAM2 - TIR domain-containing adapter molecule 2 - Homo sapiens (Human) - TICAM2 gene & protein
Functions as sorting adapter in LPS-TLR4 signaling to regulate the MYD88-independent pathway during the innate immune response to LPS. Physically bridges TLR4 and TICAM1 and functionally transmits LPS-TRL4 signal to TICAM1; signaling is proposed to occur in early endosomes after endocytosis of TLR4. May also be involved in IL1-triggered NF-kappa-B activation, functioning upstream of IRAK1, IRAK2, TRAF6, and IKBKB; however, reports are controversial. Involved in IL-18 signaling and is proposed to function as a sorting adaptor for MYD88 in IL-18 signaling during adaptive immune response.http://www.uniprot.org/uniprot/Q86XR7
Antigens, CDw218b - Medical Dictionary online-medical-dictionary.org
A subunit of the Interleukin-18 Receptor that plays a Role in receptor signaling by Association of its cytoplasmic domain with Signal Transducing Adaptor Proteins such as Myeloid Differentiation Factor 88 ...http://www.online-medical-dictionary.org/definitions-a/antigens-cdw218b.html
IL-17RC Is Required for Immune Signaling via an Extended SEF/IL-17R Signaling Domain in the Cytoplasmic Tail | The Journal of...
IL-17 has come into prominence with its identification as the signature cytokine of the Th17 lineage (32-34). However, to date the signaling mechanisms mediated by IL-17 are surprisingly poorly defined. The IL-17R family is striking in that it bears little resemblance to better known cytokine families, and thus it has not been possible to infer how this receptor mediates signals based merely on homology with other systems (6). An important clue came with the discovery of the SEFIR domain common to IL-17R family members. The homology of the SEFIR to TIR (8) was consistent with the similar panels of proinflammatory gene targets activated by IL-17 and TIR/IL-1R ligands (27). Despite this homology, the SEFIR domain is functionally and structurally distinct from TIRs. First, unlike TIR-containing receptors, IL-17R does not require the prototypical innate immune adaptors MyD88 or TRIF (9, 12). Second, SEFIR domains do not encode the BB-loop structure found in TIR domains that is required to ...http://www.jimmunol.org/content/185/2/1063.full
Caspase 9: The Suicidal Cell Whisperer | Antibody News: Novus Biologicals
Cell death via apoptosis is a key cellular function triggered by the cell death receptor family and their ligands which signal through downstream adaptor molecules and the caspase protease family.https://www.novusbio.com/antibody-news/antibodies/caspase-9-the-suicidal-cell-whisperer
STAT1 plays a role in TLR signal transduction and inflammatory responses. | Sigma-Aldrich
Sigma-Aldrich offers abstracts and full-text articles by [Kevin Luu, Claire J Greenhill, Andrea Majoros, Thomas Decker, Brendan J Jenkins, Ashley Mansell].http://www.sigmaaldrich.com/catalog/papers/25027037
The modulation of the COX process by NO represents an critical pathway that regulates the magnitude of the inflammatory method ...
The production of professional-inflammatory mediators by GM-CSF-primed BMDMs is dependent on the adaptor protein MyD88 and the nuclear translocation of NFkBp65.http://www.sgkinhibitor.com/2016/06/21/the-modulation-of-the-cox-process-by-no-represents-an-critical-pathway-that-regulates-the-magnitude-of-the-inflammatory-method/
Inhibition of the MyD88 adaptor results in reduced cyto | Open-i
Inhibition of the MyD88 adaptor results in reduced cytokine productions.PBMC from TB-IRIS patients (week 2) were treated with MyD88 inhibitor (MYD88-Inh), contrhttps://openi.nlm.nih.gov/detailedresult.php?img=PMC4595995_ncomms9451-f6&req=4
题目】白介素受体激活MYD88-ARNO-ARF6级联反应以干扰血管稳定性. 【译文】固有免疫反应对于抵御感染性疾病至关重要。巨噬细胞和其他细胞通过释放细胞因子，如白介素-1β (IL-1β)，对感染产生应答。白介素1β (IL-1β)反过来可以激活髓样分化因子88(MYD88)介导的可以引起炎症细胞激活和募集的核转录因子κB (NF-κB)依赖的转录通路。 上皮细胞通常作为炎症细胞移除血液、移入组织的屏障，它们也是炎症反应的重要调控因子。矛盾的是，对于成功免疫防御重要的细胞因子也对上皮细胞-细胞相互作用具有干扰作用，并可以触发屏障功能降低和组织结构分离。这种屏障分离的机制及其与常规NF-κB通路的关系还不十分清楚。本研究表明人体外细胞模型中IL-1β对上皮稳定性的直接、立即及破坏性作用是NF-κB非依赖的，而不是通过小GTP酶ADP核糖基化因子6 ...http://www.bioku.cn/201301/nature-interleukin-receptor-myd88-arno-arf6-cascade-vascular/
TRIF兔多克隆抗体(ab62583)可与人样本反应并经WB, IHC, ICC/IF实验严格验证，被1篇文献引用并得到1个独立的用户反馈。所有产品均提供质保服务，中国75%以上现货。http://www.abcam.cn/trif-antibody-ab62583.html
NR 3.5 84293.1
POLYRIBONUCLEOTIDE NUCLEOTIDYLTRANSFERASE, POLYRIBONUCLEOTIDE NUCLEOTIDYLTRANSFERASE, POLYRIBONUCLEOTIDE NUCLEOTIDYLTRANSFERASE, RNA, 5'-R(*UP*AP*AP*CP*UP*UP*UP*GP*GP)-3', RNA, 5'-R(*UP*AP*AP*CP*UP*UP*UP*GP*GP)-3', RNA, 5'-R(*UP*AP*AP*CP*UP*UP*UP*GP*GP)-3', RNA, 5'-R(*UP*AP*AP*CP*UP*UP*UP*GP*GP)-3 ...http://rna.bgsu.edu/rna3dhub/nrlist/view/NR_3.5_84293.1