Relevant bibliographies by topics / TLR- 3

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'TLR- 3'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "TLR- 3"

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Pineda, Antonio, S. Leticia Verdin-Terán, Ausencio Camacho, and Leticia Moreno-Fierros. "Expression of Toll-like Receptor TLR-2, TLR-3, TLR-4 and TLR-9 Is Increased in Placentas from Patients with Preeclampsia." Archives of Medical Research 42, no. 5 (July 2011): 382–91. http://dx.doi.org/10.1016/j.arcmed.2011.08.003.

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Szczepański, Mirosław, Witold Szyfter, Renata Jenek, Maciej Wróbel, Iwona Mozer Lisewska, and Jan Żeromski. "Toll-like receptors 2, 3 and 4 (TLR-2, TLR-3 and TLR-4) are expressed in the microenvironment of human acquired cholesteatoma." European Archives of Oto-Rhino-Laryngology 263, no. 7 (March 15, 2006): 603–7. http://dx.doi.org/10.1007/s00405-006-0030-1.

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TAMAKI, YASUNOBU, YUYA TAKAKUBO, TOMOYUKI HIRAYAMA, YRJÖ T. KONTTINEN, STUART B. GOODMAN, MITSUNORI YAMAKAWA, and MICHIAKI TAKAGI. "Expression of Toll-like Receptors and Their Signaling Pathways in Rheumatoid Synovitis." Journal of Rheumatology 38, no. 5 (February 15, 2011): 810–20. http://dx.doi.org/10.3899/jrheum.100732.

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Objective.Toll-like receptors (TLR) recognizing endogenous and exogenous danger signals could play a role in rheumatoid arthritis (RA). Our aim was to describe the presence, localization, and extent of expression of TLR and their adapters.Methods.TLR 1, 2, 3, 4, 5, 6, and 9 receptors, and myeloid differentiation primary response protein 88, Toll/interleukin receptor (TIR) domain-containing adapter protein MyD88 adapter-like, and TIR domain-containing adapter-inducing interferon/TIR-containing adapter molecule-1 adapters were analyzed in RA (n = 10) and osteoarthritis (OA; n = 5) samples using real-time polymerase chain reaction (PCR). Their colocalization with cellular markers CD68, CD15, CD3, CD4, CD8, CD20, dendritic cell lysosomal-associated membrane protein (DC-LAMP), CD123, and 5B5 was analyzed in double immunofluorescence staining.Results.In RA, ß-actin standardized messenger RNA of TLR 2, 3, and 9 (p < 0.001) were particularly high. TLR 5 and 6 were also elevated (p < 0.05), but TLR 1 and 4 and adapters did not differ between RA and OA. In double-staining, TLR and adapters were strongly labeled in myeloid and plasmacytoid dendritic cells (DC), moderately in CD68+ type A lining cells/macrophages, and weakly to moderately in 5B5+ type B lining cells/fibroblasts. CD3+/CD4+ and CD3+/CD8+ T cells and CD20+ B cells in perivenular areas and in lymphoid follicles were moderately TLR- and weakly adapter-positive. In OA, TLR and adapters were weakly immunolabeled in vascular, lining, and inflammatory cells.Conclusion.RA synovium showed abundant expression of TLR. RA synovitis tissue seems to be responsive to TLR ligands. DC, type A cells/macrophages, and type B cells/fibroblasts are, in that order from highest to lowest, equipped with TLR, suggesting a hierarchical responsiveness. In RA, danger-associated molecular patterns to TLR interactions may particularly drive DC to autoinflammatory and autoimmune cascades/synovitis.
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van Tongeren, Joost, Korneliusz Golebski, Danielle Van Egmond, Esther J. de Groot, Wytske J. Fokkens, and Cornelis M. van Drunen. "Synergy between TLR-2 and TLR-3 signaling in primary human nasal epithelial cells." Immunobiology 220, no. 4 (April 2015): 445–51. http://dx.doi.org/10.1016/j.imbio.2014.11.004.

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Pryimenko, Nataliia O., Tetiana M. Kotelevska, Tetiana I. Koval, Vadym A. Bodnar, Liudmyla M. Syzova, and Stanislav S. Rudenko. "EFFICACY OF SPECIFIC PREVENTION OF INFLUENZA IN INDIVIDUALS WITH POLYMORPHISMS ARG753GLN OF TLR-2, LEU412PHE OF TLR-3, ASP299GLY OF TLR-4 GENES." Wiadomości Lekarskie 73, no. 9 (2020): 1944–49. http://dx.doi.org/10.36740/wlek202009209.

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The aim: Is to study the efficacy of influenza vaccination for individuals with polymorphism Arg753Gln of TLR-2 gene, Leu412Phe of TLR-3 gene, and Asp299Gly of TLR-4 gene. Materials and methods: 66 people with mutant genotypes and normal distribution of alleles of TLR-2, TLR-3, TLR-4 genes, aged 18-63, were inoculated with anti-influenza vaccine. The genotyping of Arg753Gln polymorphic site of TLR-2, Asp299Gly of TLR-4, and Leu412Phe of TLR-3 gene was carried out by polymerase chain reaction with oligonucleotide primers usage. The immunological efficacy of vaccination was evaluated by seroconversion, seroprotection, and dynamics of mean geometric titers of antibodies. Results: It has been established that individuals with mutant genotypes Arg/Gln of TLR-2, Leu/Phe, Phe/Phe of TLR-3, Asp/Gly of TLR-4 genes have a vaccinal response to administering anti-influenza vaccine at the level of subjects with normal distribution of TLR alleles, as evidenced by the growth in dynamics of mean geometric titers of antibodies to vaccine strains, the level of seroprotection and seroconversion. Clinical and epidemiological efficacy of vaccination in this category of people is characterized by: reduction of ARI cases in the postvaccinal period by 2,0-3,0 times; prevention of pneumonia in all vaccinated subjects; decrease in the frequency of bronchitis by 2,5-3,8 times. Conclusions: Effectiveness of influenza vaccination in individuals with Arg573Gln polymorphism of TLR-2, Leu412Phe of TLR-3, Asp299Gly of TLR-4 genes by immune and clinical epidemiological parameters is determined at the level of vaccinated subjects with normal distribution of TLR-2, TLR-3, TLR-4 alleles. Specific influenza immunization of people with polymorphic modified genotypes of TLR-2, TLR-3, TLR-4 genes can prevent the development of pneumonia and reduce the incidence of bronchitis.
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Qi, Chen, Xu Xiaofeng, and Wang Xiaoguang. "Effects of Toll-Like Receptors 3 and 4 in the Osteogenesis of Stem Cells." Stem Cells International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/917168.

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Objective. To investigate the effects of Toll-like receptors in stem cell osteogenesis.Methods. Bone marrow mesenchymal stem cells (BMSCs) were divided into the blank group, the TLR-3 activated group, and the TLR-4 activated group. After 10 days’ osteogenic-promoting culture, expression of type I collagen and osteocalcin was determined by Western blot. Osteoblasts (OBs) were also divided into three groups mentioned above. Alkaline phosphatase (ALP) and alizarin red staining were performed after 10 days’ ossification-inducing culture. The expression ofβ-catenin was investigated by Western blot.Results. Both the TLR-3 and TLR-4 activated groups had increased expression of type I collagen and osteocalcin; the effect of TLR-4 was stronger. The intensity of alizarin red and ALP staining was strongest in the TLR-3 activated group and weakest in the TLR-4 activated group. Activation of TLR-4 decreased the expression ofβ-catenin, whilst activation of TLR-3 did not affect the expression ofβ-catenin.Discussion. This study suggested that both TLR-3 and -4 promoted differentiation of BMSCs to OBs. TLR-3 had an inducing effect on the ossification of OBs to osteocytes, whilst the effect of TLR-4 was the opposite because of its inhibitory effect on the Wnt signaling pathway.
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López-Haber, Cynthia, Roni Levin-Konigsberg, Yueyao Zhu, Jing Bi-Karchin, Tamas Balla, Sergio Grinstein, Michael S. Marks, and Adriana R. Mantegazza. "Phosphatidylinositol-4-kinase IIα licenses phagosomes for TLR4 signaling and MHC-II presentation in dendritic cells." Proceedings of the National Academy of Sciences 117, no. 45 (October 27, 2020): 28251–62. http://dx.doi.org/10.1073/pnas.2001948117.

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Toll-like receptor (TLR) recruitment to phagosomes in dendritic cells (DCs) and downstream TLR signaling are essential to initiate antimicrobial immune responses. However, the mechanisms underlying TLR localization to phagosomes are poorly characterized. We show herein that phosphatidylinositol-4-kinase IIα (PI4KIIα) plays a key role in initiating phagosomal TLR4 responses in murine DCs by generating a phosphatidylinositol-4-phosphate (PtdIns4P) platform conducive to the binding of the TLR sorting adaptor Toll-IL1 receptor (TIR) domain-containing adaptor protein (TIRAP). PI4KIIα is recruited to maturing lipopolysaccharide (LPS)-containing phagosomes in an adaptor protein-3 (AP-3)-dependent manner, and both PI4KIIα and PtdIns4P are detected on phagosomal membrane tubules. Knockdown of PI4KIIα—but not the related PI4KIIβ—impairs TIRAP and TLR4 localization to phagosomes, reduces proinflammatory cytokine secretion, abolishes phagosomal tubule formation, and impairs major histocompatibility complex II (MHC-II) presentation. Phagosomal TLR responses in PI4KIIα-deficient DCs are restored by reexpression of wild-type PI4KIIα, but not of variants lacking kinase activity or AP-3 binding. Our data indicate that PI4KIIα is an essential regulator of phagosomal TLR signaling in DCs by ensuring optimal TIRAP recruitment to phagosomes.
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O'Neill, Luke A. J. "TLR-7 and antiviral immunity." Trends in Immunology 23, no. 5 (May 2002): 234. http://dx.doi.org/10.1016/s1471-4906(02)02199-3.

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Wonder, Robyn, Steliana Penzkofer, and Evelyn G. Hazen. "Cardiotoxicity of anthracycline: Novel approach through down regulation of TLR-3 via TRAF/MAPK signaling pathway." American Journal of BioMedicine 2, no. 3 (June 2, 2015): 423–32. http://dx.doi.org/10.18081/2333-5106/015-02/413-422.

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Cardiotoxicity is one of the most important complications doxorubicin (DOX) and its pathomechanisms are not completely elucidated. We hypothesize that signaling via toll-like receptor (TLR)-3, a receptor that is activated upon binding of double-stranded nucleotides, might play a crucial role in the pathogenesis of cardiac-toxicity following DOX treatment. Male adult C57BL6 wild-type mice and TLR-3 knock-out (-/-) mice were subjected to 20 mg/kg; administered intraperitoneally. TLR-3 down-stream signaling was activated in WT mice lead to strong pro-inflammatory response with significant monocyte cells invasion. In contrast, this effect was attenuated in TLR-3-/- mice. Moreover, the TLR-3 activation resulted in cardiac damage that was associated with significantly reduced LV function and increased monocyte chemoattractant protein-1 (MCP)-1 expression in WT mice. This finding was confirmed by increased MAPK and TRIF protein expression in WT mice. This study confirmed that the absence of TLR-3 is associated with lower heart injury and maintained LV function. Thus, we conclude that TLR-3 seems to participate in the pathogenesis of cardiotoxicity of DOX.
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Wonder, Robyn, Steliana Penzkofer, and Evelyn G. Hazen. "Cardiotoxicity of anthracycline: Novel approach through down regulation of TLR-3 via TRAF/MAPK signaling pathway." American Journal of BioMedicine 3, no. 2 (June 2, 2015): 423–32. http://dx.doi.org/10.18081/2333-5106/015-02/423-432.

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Cardiotoxicity is one of the most important complications doxorubicin (DOX) and its pathomechanisms are not completely elucidated. We hypothesize that signaling via toll-like receptor (TLR)-3, a receptor that is activated upon binding of double-stranded nucleotides, might play a crucial role in the pathogenesis of cardiac-toxicity following DOX treatment. Male adult C57BL6 wild-type mice and TLR-3 knock-out (-/-) mice were subjected to 20 mg/kg; administered intraperitoneally. TLR-3 down-stream signaling was activated in WT mice lead to strong pro-inflammatory response with significant monocyte cells invasion. In contrast, this effect was attenuated in TLR-3-/- mice. Moreover, the TLR-3 activation resulted in cardiac damage that was associated with significantly reduced LV function and increased monocyte chemoattractant protein-1 (MCP)-1 expression in WT mice. This finding was confirmed by increased MAPK and TRIF protein expression in WT mice. This study confirmed that the absence of TLR-3 is associated with lower heart injury and maintained LV function. Thus, we conclude that TLR-3 seems to participate in the pathogenesis of cardiotoxicity of DOX.
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Dissertations / Theses on the topic "TLR- 3"

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Guillot, Loic. "Rôle des "toll-like receptor" (TLR) 3 et TLR4 dans l'immunité innée de la muqueuse pulmonaire." Paris 6, 2004. http://www.theses.fr/2004PA066147.

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Hamann, Timothy [Verfasser]. "Interaktion von TLR-3 stimuliertem retinalen Pigmentepithel und retinaler Mikroglia vor dem Hintergrund der altersabhängigen Makuladegeneration / Timothy Hamann." Kiel : Universitätsbibliothek Kiel, 2017. http://d-nb.info/114495519X/34.

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Desnous, Béatrice. "Effets de l'administration intra-hippocampique et intra-péritonéale de l'acide polyinosinique polycytidylique, agoniste des récepteurs TLR-3, sur l'épileptogenèse." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC289.

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Notre approche expérimentale a pour but d'évaluer le rôle de l'inflammation virale dans l'épileptogenèse. Nous avons choisi de modéliser l'inflammation virale par injection d'un agoniste TLR-3, acide polyinosinique polycytidylique (PIC) soit intra-péritonéale, soit intra-hippocampique, Chaque modélisation inflammatoire était couplée à un modèle d'épileptogenèse électrique le kindling rapide. L'ensemble de notre travail expérimental était réalisé chez le rat Wistar à P14 et à P75. Notre travail a montré que l'injection I. H, de PIC facilitait l'épileptogenèse du cerveau immature et adulte et induisait une augmentation du taux I. H. D'IL-1P à P14 et P75. A l'opposé la minocycline inhibait cette facilitation de l'épileptogenèse sans bloquer l'augmentation I. H. De l'IL-113 aux 2 âges étudiés. Nous avons montré que l'injection I,p, de PIC facilitait l'épileptogenèse du cerveau immature uniquement. Nous avons observé à P14 une réponse immunitaire avec une inflammation périphérique plus importante que chez l'adulte suivi d'une augmentation de l'IL-1ß hippocampique présente uniquement à P14. La BHE avait une perméabilité plus importante chez les P14 prétraités par PIC que chez l'adulte. Ces éléments nous amènent a suggérer un passage de rIL-1p de la périphérie vers le secteur intra-cérébral avec augmentation précoce et transitoire de l'IL-1ß intra-hippocampique,enforcée que nous n'avons
Our experimental approach is intended to assess the rote of viral inflammation in epileptogenesis. We chose to model the viral inflammation by 'Meeting a TLR-3 agonist, polyinosinic polycytidylic (PIC) or intraperitoneal or intra-hippocampal, Each inflammatory modeling was coupled to an electric Epileptogenesis mode rapid kindling, All of our experimental work was performed in Wistar rats at P14 and P75. Our work has shown that the injection I. H, PIC facilitated epileptogenesIs immature and adult brain and induced an increase of I. H, levels of IL-1ß to P14 and P75. In contrast minocycline inhibited this facilitation epileptogenesis without blocking I. H. Increase of IL-1ß to 2 ages studied. We have shown that the injection in PIC- facilitated epileptogenesis immature brain only. We observed an immune response to P14 with a. .
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Endoh, Yasumi Medical Sciences Faculty of Medicine UNSW. "New mechanisms modulating S100A8 gene expression." Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/42942.

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S100A8 is a highly-expressed calcium-binding protein in neutrophils and activated macrophages, and has proposed roles in myeloid cell differentiation and host defense. Functions of S100A8 are not fully understood, partly because of difficulties in generating S100A8 knockout mice. Attempts to silence S100A8 gene expression in activated macrophages and fibroblasts using RNA interference (RNAi) technology were unsuccessful. Despite establishing validated small interfering RNA (siRNA) systems, enzymaticallysynthesized siRNA targeted to S100A8 suppressed mRNA levels by only 40% in fibroblasts activated with FGF-2+heparin, whereas chemically-synthesized siRNAs suppressed S100A8 driven by an S100A8-expression vector by ~75% in fibroblasts. Suppression of the gene in activated macrophages/fibroblasts was low, and some enzymatically-synthesized siRNAs to S100A8, and unrelated siRNA to GAPDH, induced/enhanced S100A8 expression in macrophages. This indicated that S100A8 may be upregulated by type-1 interferon (IFN). IFN-β enhanced expression, but did not directly induce S100A8. Poly (I:C), a synthetic dsRNA, directly induced S100A8 through IL-10 and IFN-dependent pathways. Induction by dsRNA was dependent on RNA-dependent protein kinase (PKR), but not cyclooxygenase-2, suggesting divergent pathways in LPS- and dsRNA-induced responses. New mechanisms of S100A8 gene regulation are presented, that suggest functions in anti-viral defense. S100A8 expression was confirmed in lungs from influenza virus-infected mice and from a patient with severe acute respiratory syndrome (SARS). Multiple pathways via mitochondria mediated S100A8 induction in LPS-activated macrophages; Generation of reactive oxygen species via the mitochondrial electron transport chain and de novo synthesis of ATP may be involved. This pathway also regulated IL-10 production, possibly via PKR. Extracellular ATP and its metabolites enhanced S100A8 induction. Results support involvement of cell stress, such as transfection, in S100A8 expression. A breast tumor cell line (MCF-7) in which the S100A8 gene was silenced, was established using micro RNA technology; S100A8 induction by oncostatin M was reduced by >90% in stably-transfected cells. This did not alter MCF-7 growth. The new approach to investigate the role of S100A8 in a human tumor cell line may assist in exploring its functions and lead to new studies concerning its role in cancer.
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Fallah, Mosoka Papa. "ROLE OF PI3K-AKT PATHWAY IN THE AGE ASSOCIATED DECLINE IN TLR MEDIATED ACTIVATION OF INNATE AND ADAPTIVE IMMUNE RESPONSES." UKnowledge, 2011. http://uknowledge.uky.edu/gradschool_diss/205.

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Immunosenescence results in reduced immune response to infections with Streptococcus pneumoniae as well as to pneumococcal polysaccharide vaccines. The antibody response to the capsular polysaccharide (CPS) provides protection against S. pneumoniae infection. CPS immunoresponse is T cell independent and needs the macrophage-derived cytokines such as IL-12, IL-6 and IL-1β to elicit an antibody response. We showed a cytokine dysregulation, i.e. a decrease in IL-12, IL-6 and TNF-α but an increase in IL-10, in the aged (18-24 months old comparable to >65 years in human) compared to young adult mouse (8-12 weeks less than 65 years old) splenic macrophages (SM) or bone marrow derived macrophages (BMDM) activated via TLR4, TLR2 or TLR9 as well as heat killed Streptococcus pneumoniae (HKSP). There is also an age-associated defect in splenic B cells in the production of IgG3 upon stimulation with these ligands. A microarray analysis in SM followed by validation by both qt-RTPCR and western blots indicated that this age-associated defect in aged SM, BMDM and B cells was due to a heightened activity of the PI3K-Akt signaling pathway. We hypothesized that the senescence of immune responses in macrophages and B cells is due to an increase in activity of PI3K/Akt and decrease in the activity of GSK-3, the downstream kinase. Inhibition of the PI3-kinase with either LY294002 or Wortmannin restored the TLR2, 4, 9 and HKSP induced cytokine phenotype of the aged to that of the young adult in both the SM and BMDM and an enhanced IgG3 production in aged mice. We also showed that inhibition of glycogen synthase kinase-3 (GSK-3) the downstream target of the PI3K-Akt signaling pathway with SB216763 in SM, BMDM and B cells resulted in an enhancement in production of IL-10, IL-6 and IL-1β by macrophages and in B cell activation. Treatment of B cells with SB216763 in the presence of ligands for TLR-1/2, 4 or 9 as well as HKSP under in vitro conditions led to enhanced production of IgG3 and IgA, plasma cell formation and a slight increase in the proliferation of the B-cells with no adverse effects on the viability of the cells. Therefore, targeting the PI3K-AKT-GKS-3 signaling pathway could rescue the intrinsic signaling defect in the aged macrophages, increase IL-12 and IL-6, and enhance anti-CPS antibody responses.
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Campbell, Sara J. "Mechanisms of Moraxella catarrhalis Induced Immune Signaling in the Pulmonary Epithelium." University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1268141520.

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Salisbury, Richard L. Jr. "TCDD represses 3'IghRR activation through an AhR-dependent shift in the NF-κB/Rel protein complexes binding to κB motifs within the hs1,2 and hs4 enhancers." Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1401136335.

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Kuzemtseva, Liudmila. "Distribución tisular de los receptores Toll-like (TLR) 3, 7 y 9 en el cerdo y efecto in vitro de la infección por el virus de síndrome respiratorio y reproductivo porcino en su regulación en macrófagos alveolares porcinos." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/284490.

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Los receptores Toll-like (TLRs), en particular los que se encuentran en vesículas intracelulares de origen endosomal (TLR3, TLR7 y TLR9), están involucrados en la respuesta innata antivírica. La unión a sus respectivos ligandos conduce a la activación de cascadas intracelulares que resultan en una producción de citoquinas pro-inflamatorias (TNF-α) y antivirales (interferones de tipo I). Existe muy poca información sobre la distribución celular y tisular de estos receptores en la especie porcina así como su regulación en condiciones normales o de infección. En el primer estudio de la presente tesis se valoró la distribución tisular de los TLRs endosomales en pulmón y tejidos linfoides primarios y secundarios de cerdos sanos de distintas edades. El marcaje del TLR9 se realizó con un anticuerpo comercial con reactividad específica para el porcino. En cambio, en el caso de TLR3 y TLR7 los anticuerpos se dirigían a las moléculas humanas pero, supuestamente, poseían reactividad cruzada con las moléculas de origen porcino. Los resultados obtenidos permitieron valorar la distribución del TLR9 en los distintos tejidos examinados, pero no la de los TLR3 y TLR7 ya que el uso de los anticuerpos dirigidos frente a estos dos últimos receptores no produjo resultados satisfactorios. Así, el marcaje obtenido con el anticuerpo anti-TLR3 fue muy variable en función del tejido utilizado; es decir, en algunos órganos como el pulmón, tonsila o linfonodos parecía ser específico, pero en otros como en el hígado, producía un intenso color de fondo inespecífico. Por el contrario, sí hubo un marcaje específico para el TLR9 que reveló una expresión constitutiva de dicho receptor en células de la periferia de los folículos linfoides de los linfonodos, la tonsila y las placas de Peyer, (células de tipo epitelial, dendríticas, macrófagos o linfocitos) un hecho que sugería que este receptor probablemente puede jugar un papel importante en la activación el sistema inmunitario de los cerdos a partir de las 3 semanas de vida. El segundo estudio de esta tesis consistió en determinar la variación de la expresión de TLR3, TLR7 y TLR9 a lo largo del tiempo en una población de células presentadoras de antígeno. La población de estudio elegida fue la de macrófagos alveolares porcinos (PAMs). Los resultados de la cinética de expresión mediante citometría de flujo nos mostró que estas células presentaban una expresión basal elevada de TLR3 y TLR9 pero no de TLR7. Una de las explicaciones posibles para este marcaje basal señalaría a la necesaria manipulación de estas células antes de ser congeladas como responsable de esta expresión. Por otra parte, es difícil conocer con exactitud el ambiente en el cual se encontraban los PAMs en el pulmón antes de ser recogidos (concentración de interleuquinas, quimioquinas, otras moléculas, etc). Dado que los animales donantes estaban sanos, no presentaban ningún tipo de lesión pulmonar y eran libres de los patógenos víricos comunes del cerdo (circovirus porcino de tipo 2, influenza A y virus del PRRS entre otros) la causa de esta elevada expresión no está clara. En cuanto a la expresión de TLR7, apenas se pudo detectar una expresión basal en los PAMs utilizados. Para el tercer estudio de esta tesis se buscó un modelo de infección con un virus RNA que pudiera influir en la regulación de estos TLRs y además pudiera añadir nuevos conocimientos respecto a la inmunopatogenia de dicha infección. En el campo de las enfermedades infecciosas del porcino, una de las mayores incógnitas inmunológicas del momento la encontramos en la infección con el virus del PRRS. Los resultados de este estudio demostraron que dos cepas del mismo genotipo del virus del PRRS causaban una regulación diferente del TLR3 y del patrón de citoquinas pro-inflamatorias. En concreto, en los estudios de citometría de flujo, la cepa 3262 al inducir la expresión de TLR3 en PAMs, sobre todo a dosis elevadas (m.o.i=1), activaría la producción de TNF-α+; en cambio, la cepa 3267 o la cepa vacunal DV activaron TLR3 con menor intensidad y no inducirían TNF-α; sugiriendo en definitiva, que la regulación del patrón de citoquinas antivirales o pro-inflamatorias en los macrófagos dependería del tipo de cepa utilizada. Resulta interesante señalar que a pesar de las diferencias observadas en la citometría de flujo respecto el porcentaje de células que expresaban TLR3 y en la intensidad de su expresión según el tipo de virus utilizado, la expresión relativa del mRNA no parecía modificarse. Estas diferencias resultan interesantes y apuntan a que distintas cepas de campo de genotipo europeo podrían ejercer un efecto regulador de diferente intensidad sobre moléculas inhibitorias de la cascada de señalización de los TLRs. Además esta regulación parece depender de diferentes factores tales como: la cepa vírica, el tiempo de infección y la dosis infectiva inicial. Nuestros resultados pueden ser útiles para abrir y conducir una nueva línea de investigaciones orientadas hacia el área de la inmunidad innata frente al virus del PRRS.
Toll-like receptors (TLRs), particularly those found within intracellular vesicles of endosomal origin (TLR3, TLR7 and TLR9), are involved in the innate antiviral responses. Binding of those receptors to their respective ligands leads to the activation of intracellular cascades resulting in the release of pro-inflammatory cytokines (TNF-α) and antiviral (type I) interferons. The knowledge on the distribution of those receptors in porcine organs, tissues and cells and its regulation in physiological states or in infection is scarce. In the first study of the present thesis the distribution of endosomal TLRs in lung and primary and secondary lymphoid tissues of healthy pigs of different ages was assessed. Labeling of TLR9 was performed using a commercial antibody with specific reactivity for the porcine TLR9. For TLR3 and TLR7 the antibodies used in the study were directed to human molecules but they were supposed to cross-react with the porcine counterpart molecules. The results allowed the assessment of the distribution of TLR9 in the different tissues examined, but not that of TLR3 and TLR7 since the use of antibodies directed against the latter two receptors did not yield satisfactory results. Thus, labeling obtained with the anti-TLR3 antibody was highly variable depending on the tissue examined, that is, in some organs such as lungs, tonsils or lymph nodes labeling was apparently specific but in others, as in the liver, the se of that antibody resulted in an intense non-specific background. By contrast, TLR9 labeling was specific and revealed a constitutive expression of this receptor in cells of the periphery of lymphoid follicles of lymph nodes, tonsils and Peyer's patches (epithelial cells, dendritic cells, macrophages or lymphocytes) a fact suggesting that this receptor can probably play an important role in activating the immune system of pigs of 3 week-old piglets. The second study of this thesis was aimed to determine the variation of the expression of TLR3, TLR7 and TLR9 over time in a population of antigen-presenting cells. Porcine alveolar macrophages (PAMs) were used for this purpose. The results of the kinetics of expression as assessed by flow cytometry showed that PAMs had a high basal expression of TLR3 and TLR9 but not of TLR7. A possible explanation for this basal labeling could point to the unavoidable manipulation of PAMs needed for their collection. Moreover, it is difficult to know precisely the environmental conditions in which PAMs were in the lungs before being collected (concentration of interleukins, chemokines, presence of other molecules, etc.). Since PAM donors were healthy, showed no lung lesions and were demonstrated to be free of common viral pathogens of pigs (porcine circovirus type 2, influenza A and PRRS virus among others) the cause of this elevated expression remains unclear. As for TLR7, basal expression in the PAMs used was low or nil. The third study of the present thesis aimed to a model of infection with an RNA virus that might influence the regulation of these TLRs and also could add new knowledge regarding the pathogenesis of the infection. In the field of infectious diseases of swine, one of most interesting models of RNA virus infections is PRRS virus for which immunopathogenesis is largely understood. The results of this study showed that two strains of the same genotype of PRRS virus resulted in a different regulation of TLR3 and in a different pattern of pro-inflammatory cytokines. Specifically, in flow cytometry experiments, strain 3262, induced the expression of TLR3 in PAMs, particularly at high multiplicities of infection (m.o.i = 1) and triggered the production of TNF-α+ whereas strain 3267 or the vaccine strain DV resulted in lower TLR3 expression and did not induce TNF-α, suggesting ultimately that the regulation of the antiviral or pro-inflammatory cytokine patterns in macrophages depends on the strain used. Interestingly, despite the differences observed in flow cytometry for TLR3, the relative mRNA expression did not apparently change under different circumstances. This was an interesting observation that suggests that different field strains of genotype I PRRSV might exert a regulatory effect of different intensity on inhibitory molecules of the signaling cascade of TLRs. Furthermore, this regulation seems to depend on various factors such as the viral strain, the time of infection and the multiplicity of infection. Our results may be useful as a basis for further studies in the area of innate immunity against PRRS virus.
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Liljeroos, M. (Mari). "Toll-like receptor 2 (TLR2) and TLR4 signaling in the innate response against bacterial components." Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514288111.

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Abstract Toll-like receptors (TLRs) are transmembrane proteins involved in the recognition of specific microbial structures and thus the activation of signaling cascades of innate immunity. Regulation of the innate immune response is a complex biological process involving the combined synergistic and antagonistic effects of distinct signaling mediators. Although TLR signaling has been widely studied in recent years, there remain many unexplored unique features of each TLR signaling pathway. The present study evaluated the activation and regulation of TLR4 and TLR2 signaling with the aim of better understanding the molecular mechanisms that control these inflammatory signaling pathways. In the present study, the signal transduction mechanisms of TLR4 and TLR2 in response to Escherichia coli LPS and Staphylococcus aureus LTA were evaluated in mouse macrophages. The inductions, interactions, and activations of the signaling molecules and mediators in the TLR pathways were studied by using several molecular biology and protein chemistry methods. In addition, the role of TLR4 and TLR2 in the regulation of the hepatic inflammatory reaction during endotoxemia was studied. Mouse macrophages were found to induce central proinflammatory mediators in response to LPS and LTA stimulation. Specific roles for PI 3-kinase and Btk were described. These kinases were found to be activated by LPS and LTA; moreover, PI 3-kinase and Btk were found to form specific interactions with TLRs and their intracellular signaling mediators. In addition, a unique IRF2 signaling pathway for LTA-induced TLR2 was found, resulting in the activation of signal transducers and activators of transcription (Stats) and IFN-α secretion. The secreted IFN-α was shown to regulate the LTA-induced inflammatory responses, thereby combining the LTA-induced IRF proteins into NF-κB pathway. The present study provides insight into the signal transduction mechanisms of TLRs. The understanding of these molecular mechanisms that control the activation of TLR signaling cascades will in the future help to predict predisposition and outcome in infectious diseases, and to control the course of disease at an earlier stage
Tiivistelmä Toll:n kaltaiset reseptorit (TLR) ovat solukalvon proteiineja, jotka tunnistavat taudinaiheuttajien eli patogeenien spesifisiä rakenteita johtaen elimistön puolustusjärjestelmän, immuniteetin, aktivoitumiseen. Immuniteetin säätely on monimutkainen biologinen prosessi, joka tapahtuu kudosten, solujen ja erilaisten synnynnäiseen immuniteettiin liittyvien molekyylien vuorovaikutuksina. Tulehdusvasteen säätelyssä tasapaino positiivisten ja negatiivisten säätelysignaalien välillä on erittäin tärkeää, jotta autoimmuunisairauksien, akuuttien tai kroonisten tulehdusten sekä infektiosairauksien synty voitaisiin välttää. Tämän tutkimuksen tavoitteena oli saada lisätietoa TLR2 ja TLR4 proteiinien säätelemistä signaalireiteistä, niiden vasteista tiettyjä patogeenirakenteita vastaan ja ymmärtää paremmin synnynnäisen immuniteetin puolustusmekanismeja. Patogeenirakenteiden aiheuttamaa tulehdusvastetta tutkittiin pääosin soluviljelymallissa. Lisäksi selvitettiin immuunivasteen luonnetta fysiologisessa kokonaisuudessa ja sen korrelaatiota solutasolla nähtyihin vasteisiin käyttäen in vivo hiirimallia. Tutkimus tehtiin käyttäen useita molekyylibiologian ja proteiinikemian menetelmiä proteiini- ja mRNA-ekspressioiden sekä proteiini-interaktioiden tutkimiseen ja erilaisten aktiivisuuksien määrityksiin. Tulehdusvastetta tutkittiin etenkin sytokiinivastetta määrittämällä ja signaaliketjujen toimintaa analysoitiin estämällä spesifisesti niiden toimintaa. Tarkoituksena oli selvittää, mitkä tekijät ovat välttämättömiä kyseisten tulehdusta aiheuttavien bakteerien tunnistuksessa ja puolustusreaktiossa niitä vastaan. Tutkimuksessa havaittiin kahden kinaasin, PI 3-kinaasin ja Brutonin tyrosiinikinaasin, liittyvän oleellisesti TLR signaalireitteihin. Nämä TLR:ien stimulaation seurauksena aktivoituneet kinaasit muodostivat spesifisiä sidoksia TLR:ien ja niiden signaaliketjuihin liittyvien solunsisäisten signaalivälittäjien kanssa. Lisäksi TLR2 signaalireitillä havaittiin aktivoituvan tekijöitä, jotka johtivat interferoni-α välitteiseen tulehdusvasteen säätelyyn. TLR signaalireittien selvittäminen auttaa ymmärtämään tulehdussairauksien patofysiologiaa ja voi siten tulevaisuudessa johtaa parempien hoitomenetelmien kehittämiseen
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Rao, Bhalchandra Shantikumar. "Diverse Biological Functions For 3'-5' Nucleotide Addition Reactions: tRNA Repair to tRNAHis Identity." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1397425994.

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Books on the topic "TLR- 3"

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Zuffi, Marco, ed. Societas herpetologica italica. Atti del V congresso nazionale, Calci (Pisa), 29 settembre-3 ottobre 2004. Florence: Firenze University Press, 2006. http://dx.doi.org/10.36253/88-8453-420-8.

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This book contains the proceedings of the Congress, thus making available the extensive range of research performed and in progress. The contributions, in synthetic form, illustrate the methods and results, with the support of data, tables and bibliographies, of 35 studies carried out by research teams of biologists from the universities of Roma-Sapienza, Roma Tor Vergata, Florence, Naples, Turin, Milan, Palermo, Genoa, Pisa, Padua, Pavia, Perugia and Calabria, as well as various museums, study centres, reserves and nature parks.
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Bauer, Stefan, and Gunther Hartmann, eds. Toll-Like Receptors (TLRs) and Innate Immunity. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-72167-3.

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Klein, Michael, H. D. Schulte, and E. Gams, eds. TMLR Management of Coronary Artery Diseases. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72134-2.

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Mercuri, Louis G., ed. Temporomandibular Joint Total Joint Replacement – TMJ TJR. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-21389-7.

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Ait Ameur, Yamine, and Klaus-Dieter Schewe, eds. Abstract State Machines, Alloy, B, TLA, VDM, and Z. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-43652-3.

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Micheau, Olivier, ed. TRAIL, Fas Ligand, TNF and TLR3 in Cancer. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56805-8.

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Butler, Michael, Klaus-Dieter Schewe, Atif Mashkoor, and Miklos Biro, eds. Abstract State Machines, Alloy, B, TLA, VDM, and Z. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33600-8.

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Butler, Michael, Alexander Raschke, Thai Son Hoang, and Klaus Reichl, eds. Abstract State Machines, Alloy, B, TLA, VDM, and Z. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91271-4.

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Congreso Nacional de Historia del Papel en España (5th 2003 Sarrià de Ter, Spain). Actas del V Congreso Nacional de Historia del Papel en España: Sarrià de Ter, Girona, 2, 3 y 4 de octubre de 2003. Girona: CCG Ediciones, 2003.

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Bi, Yunchen. Study of the Calcium Regulation Mechanism of TCR Activation Using Nanodisc and NMR Technologies. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-54618-5.

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Book chapters on the topic "TLR- 3"

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Stasi, Alessandra, Rossana Franzin, Giuseppe Stefano Netti, Elena Ranieri, Loreto Gesualdo, Giovanni Stallone, and Giuseppe Castellano. "TLR-4 Signaling in Pericytes." In Stem Cell Biology and Regenerative Medicine, 165–87. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62129-2_7.

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Neagu, Monica, and Carolina Constantin. "Signal Transduction in Immune Cells and Protein Kinases." In Advances in Experimental Medicine and Biology, 133–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-49844-3_5.

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AbstractImmune response relies upon several intracellular signaling events. Among the protein kinases involved in these pathways, members of the protein kinase C (PKC) family are prominent molecules because they have the capacity to acutely and reversibly modulate effector protein functions, controlling both spatial distribution and dynamic properties of the signals. Different PKC isoforms are involved in distinct signaling pathways, with selective functions in a cell-specific manner.In innate system, Toll-like receptor signaling is the main molecular event triggering effector functions. Various isoforms of PKC can be common to different TLRs, while some of them are specific for a certain type of TLR. Protein kinases involvement in innate immune cells are presented within the chapter emphasizing their coordination in many aspects of immune cell function and, as important players in immune regulation.In adaptive immunity T-cell receptor and B-cell receptor signaling are the main intracellular pathways involved in seminal immune specific cellular events. Activation through TCR and BCR can have common intracellular pathways while others can be specific for the type of receptor involved or for the specific function triggered. Various PKC isoforms involvement in TCR and BCR Intracellular signaling will be presented as positive and negative regulators of the immune response events triggered in adaptive immunity.
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Alpuente, María, Demis Ballis, Javier Espert, and Daniel Romero. "Model-Checking Web Applications with Web-TLR." In Automated Technology for Verification and Analysis, 341–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-15643-4_25.

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Martín, Óscar, Alberto Verdejo, and Narciso Martí-Oliet. "Model Checking TLR* Guarantee Formulas on Infinite Systems." In Specification, Algebra, and Software, 129–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54624-2_7.

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Balistreri, Carmela Rita, Giuseppina Candore, and Calogero Caruso. "Role of TLR Polymorphisms in Aging and Age-Related Diseases." In Handbook of Immunosenescence, 1091–107. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99375-1_34.

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Balistreri, Carmela Rita, Giuseppina Candore, and Calogero Caruso. "Role of TLR Polymorphisms in Aging and Age-Related Diseases." In Handbook of Immunosenescence, 1–18. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64597-1_34-1.

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von Stebut, Esther. "Dendritische Zellen 2008: Verschiedene DC Subtypen, TLR-Profile und neue Zytokine." In Fortschritte der praktischen Dermatologie und Venerologie, 3–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-77148-7_1.

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Compte, Nathalie, Thierry Pepersack, and Stanislas Goriely. "Frailty in Old Age Is Associated with Altered Cytokine Production in Response to TLR Ligation." In Handbook of Immunosenescence, 2417–34. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99375-1_152.

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Compte, Nathalie, Thierry Pepersack, and Stanislas Goriely. "Frailty in Old Age is Associated with Altered Cytokine Production in Response to TLR Ligation." In Handbook of Immunosenescence, 1–18. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64597-1_152-1.

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Hornung, Veit, Winfried Barchet, Martin Schlee, and Gunther Hartmann. "RNA Recognition via TLR7 and TLR8." In Toll-Like Receptors (TLRs) and Innate Immunity, 71–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-72167-3_4.

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Conference papers on the topic "TLR- 3"

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Zhang, Wenqiu, Hyunjoon Kim, Vidhi Khanna, David M. Ferguson, Thomas Griffith, and Jayanth Panyam. "Abstract 4985: TLR agonists for anticancer immunotherapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4985.

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Zhang, Wenqiu, Hyunjoon Kim, Vidhi Khanna, David M. Ferguson, Thomas Griffith, and Jayanth Panyam. "Abstract 4985: TLR agonists for anticancer immunotherapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4985.

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Stolberg-Stolberg, J., A. Böttcher, M. Sambale, J. Sherwood, MJ Raschke, T. Pap, and J. Bertrand. "Inhibition des TLR-3 Signalwegs schützt vor post-traumatischer Arthrose." In Deutscher Kongress für Orthopädie und Unfallchirurgie. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1717815.

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Takeoka, Tomohira, Hirotsugu Nagase, Yasuhiro Miyazaki, Tsuyoshi Takahashi, Yukinori Kurokawa, Tomoki Makino, Makoto Yamasaki, et al. "Abstract A169: NY-ESO-1 protein cancer vaccine with TLR 3 and 4 agonists." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-a169.

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Suresh, Madathilparambil V., Matthew D. Bender, Bi Yu, David Machado-Aranda, Beth B. Moore, and Krishnan Raghavendran. "Toll Like Receptor-3 (TLR-3) Is Required For Acute Inflammatory Response And Injury In Mice Following Lung Contusion." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1326.

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Aryee, Ken-Edwin, Lisa Burzenski, Dale Greiner, Giles F. Whalen, Leonard Shultz, James Keck, and Michael Brehm. "Abstract 1522: NovelNOD-scid IL2rgnull(NSG)mice for preclinical evaluation of TLR agonists in cancer immunotherapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1522.

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Aryee, Ken-Edwin, Lisa Burzenski, Dale Greiner, Giles F. Whalen, Leonard Shultz, James Keck, and Michael Brehm. "Abstract 1522: NovelNOD-scid IL2rgnull(NSG)mice for preclinical evaluation of TLR agonists in cancer immunotherapy." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1522.

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Haria, Dhwani, Helena Kiefel, Yuliya Katlinskaya, Sunit Jain, Thomas Weinmaier, Shoko Iwai, Todd DeSantis, Toshi Takeuchi, Karim Dabbagh, and Kareem Graham. "Abstract 1490: Novel microbiome-derived peptides activate the host innate immune system by regulation of TLR signaling." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1490.

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Haria, Dhwani, Helena Kiefel, Yuliya Katlinskaya, Sunit Jain, Thomas Weinmaier, Shoko Iwai, Todd DeSantis, Toshi Takeuchi, Karim Dabbagh, and Kareem Graham. "Abstract 1490: Novel microbiome-derived peptides activate the host innate immune system by regulation of TLR signaling." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1490.

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Sa, Y. A. P. J., N. S. B. Ribeiro, T. P. T. Ferreira, M. Hohmann, M. S. Espindola, J. C. Alves-Filho, M. A. Martins, C. M. Hogaboam, and P. M. Silva. "Role of Toll-Like Receptor (TLR)3 in Lung Fibrosis Triggered by Silica Particles in Mice." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2642.

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Reports on the topic "TLR- 3"

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Struckmeyer, R. NRC TLD Direct Radiation Monitoring Network. Progress report, July--September 1993: Volume 13, No. 3. Office of Scientific and Technical Information (OSTI), November 1993. http://dx.doi.org/10.2172/10108304.

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Struckmeyer, R. NRC TLD direct radiation monitoring network: Progress report, July--September 1997. Volume 17, Number 3. Office of Scientific and Technical Information (OSTI), January 1998. http://dx.doi.org/10.2172/569100.

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Struckmeyer, R. NRC TLD direct radiation monitoring network: Volume 15, No. 3. Progress report, July--September 1995. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/193651.

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Witt, D. C. Am/Cm TTR testing -- 3/8-inch glass beads evaluation in CIM5[Technical Task Request]. Office of Scientific and Technical Information (OSTI), January 2000. http://dx.doi.org/10.2172/750865.

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Dresner, L. The superfluid diffusion equation S(T)(@T/@t) = nabla ter dot (K(T)( nabla T) sup 1/3 ). Office of Scientific and Technical Information (OSTI), June 1990. http://dx.doi.org/10.2172/6702252.

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J. Cunningham and J. Shank. Guidelines for Electromagnetic Interference Testing of Power Plant Equipment: Revision 3 to TR-102323. Office of Scientific and Technical Information (OSTI), November 2004. http://dx.doi.org/10.2172/837279.

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Auerbach, E. A 3/2 LAMBDA BUMP TO CORRECT AGS ORBIT DISTORTION AT THE K17 GAMMA-TR QUAD. Office of Scientific and Technical Information (OSTI), May 1994. http://dx.doi.org/10.2172/1151302.

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Fisk, B. E., and D. A. Timian. In-Tank Precipitation Facility (ITP) and H-Tank Farm (HTF) geotechnical report, WSRC-TR-95-0057, Revision 0, Volume 3. Office of Scientific and Technical Information (OSTI), June 1995. http://dx.doi.org/10.2172/125432.

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Talbot, A. F., J. R. Swesey, and L. G. Magill. Turbine Fuels from Tar Sands Bitumen and Heavy Oil. Volume 2. Phase 3. Process Design Specifications for a Turbine Fuel Refinery Charging San Ardo Heavy Crude Oil. Fort Belvoir, VA: Defense Technical Information Center, September 1987. http://dx.doi.org/10.21236/ada190120.

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Miller, D., P. L. Richards, W. Y. Lee, N. Newman, S. M. Garrison, and J. S. Martens. Infrared phonon structure in epitaxial films of Tl sub 2 Ca sub 2 Ba sub 2 Cu sub 3 O sub 10 at low temperatures. Office of Scientific and Technical Information (OSTI), February 1992. http://dx.doi.org/10.2172/5001494.

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