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Published: 4 June 2021
Last updated: 1 February 2022

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1

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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2

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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3

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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5

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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6

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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7

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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8

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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9

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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11

Zhu, Yanjuan, Ahmer Kodvawala, and David Y. Hui. "Apolipoprotein E inhibits Toll-like receptor (TLR)-3- and TLR-4-mediated macrophage activation through distinct mechanisms." Biochemical Journal 428, no. 1 (April 28, 2010): 47–54. http://dx.doi.org/10.1042/bj20100016.

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Previous studies have shown that apoE (apolipoprotein E) expression in macrophages suppresses inflammatory responses; however, whether endogenously synthesized apoE acts intracellularly or after its secretion in suppressing macrophage inflammation remains unclear. The present study used the murine monocyte macrophage cell line RAW 264.7 to examine the influence of exogenous apoE on macrophage inflammatory responses induced by TLR (Toll-like receptor)-4 and TLR-3 agonists LPS (lipopolysaccharide) and poly(I-C) respectively. Results showed that exogenously added apoE suppressed the LPS and poly(I-C) induction of IL (interleukin)-6, IL-1β and TNF-α (tumour necrosis factor-α) secretion by RAW 264.7 cells. The mechanism was related to apoE suppression of TLR-agonist-induced phosphorylation of JNK (c-Jun N-terminal kinase) and c-Jun. A peptide containing the tandem repeat sequence of the receptor-binding domain of apoE, apoE-(141–155)2, was similarly effective in inhibiting LPS- and poly(I-C)-induced macrophage inflammatory responses. Reductive methylation of lysine residues in apoE, which abolished its receptor-binding capability without affecting its ability to interact with HSPGs (heparin sulfate proteoglycans), inhibited the ability of apoE to suppress macrophage responses to LPS, but had no effect on apoE suppression of poly(I-C)-induced macrophage activation. The ability of apoE to suppress poly(I-C)-induced pro-inflammatory cytokine production was abolished by heparinase treatment of RAW 264.7 cells to remove cell-surface HSPGs. Taken together, these results indicate that exogenous apoE inhibits macrophage inflammatory responses to TLR-4 and TLR-3 agonists through distinct mechanisms related to receptor and HSPG binding respectively, and that these inhibitory effects converged on suppression of JNK and c-Jun activation which are necessary for macrophage activation.
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12

Barreto, Gonçalo, Tarvo Sillat, Antti Soininen, Pekka Ylinen, Abdelhakim Salem, Yrjö T. Konttinen, Ahmed Al-Samadi, and Dan C. E. Nordström. "Do Changing Toll-like Receptor Profiles in Different Layers and Grades of Osteoarthritis Cartilage Reflect Disease Severity?" Journal of Rheumatology 40, no. 5 (March 15, 2013): 695–702. http://dx.doi.org/10.3899/jrheum.121159.

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Objective.Cartilage degeneration in osteoarthritis (OA) leads to release of potential danger signals. The aim of our study was to profile OA cartilage for the Toll-like receptor (TLR) danger signal receptors.Methods.Osteochondral cylinders from total knee replacements were graded using OA Research Society International score and stained for proteoglycans, collagenase-cleaved type II collagen, and TLR 1–10, which were analyzed histomorphometrically.Results.Grade 1 OA lesions contained 22%–55% TLR 1–9-positive cells in the surface zone, depending on the TLR type. In Grade 2 TLR, immunoreactivity was 60%–100% (p < 0.01) and it was even higher in Grades 3 and 4 (p < 0.01 vs Grade 1). TLR-positive cells in Grade 1 middle zone were low, 0–19.9%, but were 5.1%–32.7% in Grade 2 (p < 0.01) and 34%–83% in Grades 3–4 samples (p < 0.001). TLR values in Grade 5 were low (14.3%–28.7%; p < 0.001). In Grades 3–4 OA, cartilage matrix stained strongly for TLR. In Grade 1, COL2-3/4M was restricted to chondrocytes, but was increasingly seen in matrix upon progress of OA to Grade 4, and then declined.Conclusion.Cells in the gliding surface zone are fully equipped with TLR in mild OA. Their proportion increases and extends to the middle or even the deep zone, reflecting OA progression. COL2A-3/4M staining suggests Endo180-mediated intake for intralysosomal degradation by cathepsins in Grade 1, but in higher grades this chondrocyte-mediated clearance fails and the matrix demonstrates extensive collagenase-induced damage. Detached and/or partially degraded matrix components can then act as endogenous danger signals (damage-associated molecular patterns or DAMP) and stimulate increasingly TLR-equipped chondrocytes to inflammation. At the peak inflammatory response, soluble TLR may exert negative feedback, explaining in part the low TLR levels in Grade 5 OA.
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Priyam, Manisha, Mamta Tripathy, Umesh Rai, and Soma Mondal Ghorai. "Divergence of protein sensing (TLR 4, 5) and nucleic acid sensing (TLR 3, 7) within the reptilian lineage." Molecular Phylogenetics and Evolution 119 (February 2018): 210–24. http://dx.doi.org/10.1016/j.ympev.2017.11.018.

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14

Hayashi, Kozaburo, Laura C. Hooper, Marian S. Chin, Chandrasekharam N. Nagineni, Barbara Detrick, and John J. Hooks. "Herpes simplex virus 1 (HSV-1) DNA and immune complex (HSV-1–human IgG) elicit vigorous interleukin 6 release from infected corneal cells via Toll-like receptors." Journal of General Virology 87, no. 8 (August 1, 2006): 2161–69. http://dx.doi.org/10.1099/vir.0.81772-0.

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Toll-like receptor 3 (TLR-3) and TLR-9 gene expression and interleukin 6 (IL-6) secretion were studied in corneal cells with components of herpes simplex virus (HSV). Human corneal epithelial cells (HCEs) and primary human corneal fibroblasts (HCRFs) were infected with live HSV or UV-inactivated HSV (UV-HSV), transfected with HSV DNA or treated with HSV–anti-HSV IgG immune complexes. Gene expression of TLR-3 and -9 was analysed by real-time PCR. Supernatants were assayed for IL-6 by ELISA. Incubation of HCEs and HCRFs with live HSV-1, UV-HSV and HSV DNA resulted in augmented TLR-3 and -9 gene expression and IL-6 release. Moreover, infected or transfected HCRFs released greater amounts of IL-6 than did HCEs. As virus is frequently in the form of neutralized virus immune complexes, the ability of these immune complexes to interact with TLRs and trigger IL-6 production was evaluated. Here, it is shown that HSV–anti-HSV IgG complexes were as potent as HSV DNA in their ability to induce IL-6. Treatment of HCRFs transfected with HSV DNA with the TLR-9-inhibitory oligomer iODN, anti-TLR-3 antibody or phosphatidylinositol 3-kinase inhibitor indicated that IL-6 release from HCRFs was mediated by TLR-3 and -9 gene expression. These results demonstrated that neutralized HSV immune complexes were as potent as HSV DNA in enhancing IL-6 release from corneal fibroblasts. These phenomena were mediated via augmented TLR-3 and -9 gene expression.
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Karatas, A., R. F. Akkoc, and S. S. Koca. "AB0134 SERUM LL-37, GALECTIN-3, AND TOLL-LIKE RECEPTORS-3 LEVELS DECREASE IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1368.3–1368. http://dx.doi.org/10.1136/annrheumdis-2020-eular.5782.

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Background:Systemic lupus erythematosus (SLE) is a systemic inflammatory disease characterized by heterogeneous clinical manifestations (1). Although there are significant developments with its pathogenesis, it is still not fully known. In recent years, pathways such as NETosis and plasmacytoid dendritic cell (pDC) activation have been emphasized in the pathogenesis of SLE (2, 3).Objectives:In our study, we aimed to investigate serum LL-37, Galectin-3, and Toll-like receptors-3 (TLR)-3 levels, which are thought to be related to pathogenetic pathways in SLE patients.Methods:17 SLE patients and 33 healthy controls were included in the study. The clinical and laboratory features of the patients were determined. Serum LL-37, Galectin-3, and TLR-3 levels were determined by ELISA (enzyme-linked immunosorbent assay) method using the appropriate commercial kit, and the results were evaluated according to the manufacturer’s instructions.Results:The clinical and laboratory features of the groups are described in Table 1. In our study, serum LL-37, Galectin-3, and TLR-3 levels were decreased statistically significantly in SLE patients compared to healthy control (p = 0.007, p = 0.002, and p = 0.008, respectively).Table 1.Clinical and laboratory features of the groups in the studyHealthy control (n=33)SLE(n=17)pAge (years)34.1 ± 3.740 ± 11.40.05Sex (n; female/male)33/017/0LL-37(ng/ml)78.6 ± 92.614.2 ± 19.30.007Galectin-3 (ng/ml)25.5 ± 23.26.7 ± 7.60.002Toll-like receptors-3 (pg/ml)7893.4 ± 1041.3916.2 ± 469.70.008Conclusion:It is suggested that LL-37, galectin-3, and TLR-3 levels have various effects on NEtosis and pDc activation pathways in SLE pathogenesis. In our study, low levels of serum LL-37, galectin-3, and TLR-3 in SLE patients suggest that they are associated with SLE pathogenesis.References:[1]Aringer M, Schneider M. [Systemic lupus erythematosus]. Dtsch Med Wochenschr.2016;141:537-43.[2]Panda SK, Kolbeck R, Sanjuan MA. Plasmacytoid dendritic cells in autoimmunity. Curr Opin Immunol. 2017;44:20-25.[3]van der Linden M, van den Hoogen LL, Westerlaken GHA, Fritsch-Stork RDE, van Roon JAG, Radstake TRDJ, Meyaard L. Neutrophil extracellular trap release is associated with antinuclear antibodies in systemic lupus erythematosus and anti-phospholipid syndrome. Rheumatology (Oxford). 2018;57:1228-1234.Disclosure of Interests:None declared
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Collins, Patricia E., Domenico Somma, David Kerrigan, Felicity Herrington, Karen Keeshan, Robert J. B. Nibbs, and Ruaidhrí J. Carmody. "The IκB-protein BCL-3 controls Toll-like receptor-induced MAPK activity by promoting TPL-2 degradation in the nucleus." Proceedings of the National Academy of Sciences 116, no. 51 (November 26, 2019): 25828–38. http://dx.doi.org/10.1073/pnas.1900408116.

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Proinflammatory responses induced by Toll-like receptors (TLRs) are dependent on the activation of the NF-ĸB and mitogen-activated protein kinase (MAPK) pathways, which coordinate the transcription and synthesis of proinflammatory cytokines. We demonstrate that BCL-3, a nuclear IĸB protein that regulates NF-ĸB, also controls TLR-induced MAPK activity by regulating the stability of the TPL-2 kinase. TPL-2 is essential for MAPK activation by TLR ligands, and the rapid proteasomal degradation of active TPL-2 is a critical mechanism limiting TLR-induced MAPK activity. We reveal that TPL-2 is a nucleocytoplasmic shuttling protein and identify the nucleus as the primary site for TPL-2 degradation. BCL-3 interacts with TPL-2 and promotes its degradation by promoting its nuclear localization. As a consequence,Bcl3−/−macrophages have increased TPL-2 stability following TLR stimulation, leading to increased MAPK activity and MAPK-dependent responses. Moreover, BCL-3–mediated regulation of TPL-2 stability sets the MAPK activation threshold and determines the amount of TLR ligand required to initiate the production of inflammatory cytokines. Thus, the nucleus is a key site in the regulation of TLR-induced MAPK activity. BCL-3 links control of the MAPK and NF-ĸB pathways in the nucleus, and BCL-3–mediated TPL-2 regulation impacts on the cellular decision to initiate proinflammatory cytokine production in response to TLR activation.
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Aydin, U., B. Oz, A. Karatas, M. Gur, R. Piskin Sagir, G. Artas, S. Aydin, and S. S. Koca. "AB1039 LL-37, IL-36, GALECTIN-3 AND TLR-3 LEVELS IN IDIOPATHIC GRANULOMATOUS MASTITIS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1811.2–1811. http://dx.doi.org/10.1136/annrheumdis-2020-eular.5806.

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Background:Idiopathic granulomatous mastitis (IGM) is a non-infectious inflammatory disorder of the breast characterized by non-caseous granulomas. It is a chronic granulomatous inflammatory disease frequently seen in young fertile women, the cause of which has not been clearly understood. Immunosuppressive agents and surgical interventions are used in the treatment.LL-37 is a cathelicidin-derived antimicrobial peptide with immunomodulatory properties that are effective in innate immunity. In addition, IL-36, galectin-3, TLR-3 are effective in autoimmunity with proinflammatory properties.Objectives:With this study, we aimed to investigate the potential alterations of LL-37, IL 36, Galectin 3 and TLR-3 levels in IGM.Methods:35 female patients with biopsy-confirmed IGM and 35 healthy controls were included in the study. The serum samples of the subjects LL-37, IL 36, Galectin 3 and TLR-3 levels were studied using the Elisa method. While studying LL 37 and Galectin 3 levels in the tissue, samples of 10 patients who underwent mammoplasty for cosmetic reasons were used for the control group. Ten patients whose paraffin blocks were eligible for re-study were included in the study for tissue examinations. Based on the prevalence (0.1: <%25,- 0.4:%26-50, 0.6:%51-75, 0.9:%76-100) and severity (0: no, +0.5: very little, +1: little, +2: medium, +3: severe) of immunoreactivity in staining, histoscore was created (histoscores = prevalence x severity).The data were evaluated using appropriate statistical analysis and p <0.05 was considered statistically significant.Results:When the patient and control groups included in the study were compared, there was no significant difference in age. In serum samples, LL 37, IL 36, Galectin 3 and TLR 3 levels were statistically significantly lower in IGM group compared to the control group (p <0.001 for each) (Table-1). In biopsy samples, LL 37 level was found to be significantly lower in IGM group compared to the control group (p <0.001). However, no significant difference was detected in Galectin 3 levels in tissue studies (Table-2).Conclusion:In our study, we found that the levels of LL 37, IL 36, Galectin 3 and TLR 3 decreased in serum samples in IGM disease whose etiology was not clearly understood. In addition, we showed that in patients with IGM, LL 37 levels decreased at the tissue level. Studies have shown that in cases of severe sarcoidosis, LL 37 deficiency is reduced both in level and gene expression. So they thought, deficiency of cathelicidin LL 37 may impede resolution of inflammation in the tissue of patients with severe form disease.References:[1]Barna, Barbara P et al. “Alveolar macrophage cathelicidin deficiency in severe sarcoidosis.” Journal of innate immunity vol. 4,5-6 (2012): 569-78.[2]Al-Khaffaf, Bilal et al. “Idiopathic granulomatous mastitis: a 25-year experience.” Journal of the American College of Surgeons vol. 206,2 (2008): 269-73.Table 1.LL 37, IL 36, Galectin 3 and TLR 3 levels in serum samplesIGM(N:35)CONTROL (N:35)PAge35,92 ± 5,1934,03 ± 3,810,08LL 37 (ng/ml)5,20 ± 5,4840,05 ± 31,97<0,001IL 36 (pg/ml)294,74 ± 125,94864,71 ± 442,39<0,001Galectin 3 (ng/ml)3,61 ± 3,1615,53 ± 10,14<0,001TLR 3 (pg/ml)931,49 ± 443,864019,36 ± 2599,51<0,001IGM: Idiopathic granulomatous mastitisTable 2.Evaluation of LL-37 and Galectin 3 levels with histoscores in biopsy samplesIGM (N:10)CONTROL (N:10)PLL 370,006 ± 0,0250,140 ± 0,516<0,001Galectin 30,293 ± 0,2010,400 ± 0,2900,32Disclosure of Interests:None declared
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Turaj, Anna H., Lekh N. Dahal, Stephen A. Beers, Mark S. Cragg, and Sean H. Lim. "TLR-3/9 Agonists Synergize with Anti-ErbB2 mAb—Letter." Cancer Research 77, no. 12 (June 5, 2017): 3376–78. http://dx.doi.org/10.1158/0008-5472.can-17-0412.

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Hu, Yun‐Hong, Yu Zhang, Li‐Qun Jiang, Shuai Wang, Cao‐Qi Lei, Ming‐Shun Sun, Hong‐Bing Shu, and Yu Liu. "WDFY 1 mediates TLR 3/4 signaling by recruiting TRIF." EMBO reports 16, no. 4 (March 3, 2015): 447–55. http://dx.doi.org/10.15252/embr.201439637.

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Wang, Bo, Kaori Koga, Yutaka Osuga, Ingrid Cardenas, Gentaro Izumi, Masashi Takamura, Tetsuya Hirata, et al. "Toll-Like Receptor-3 Ligation-Induced Indoleamine 2, 3-Dioxygenase Expression in Human Trophoblasts." Endocrinology 152, no. 12 (September 27, 2011): 4984–92. http://dx.doi.org/10.1210/en.2011-0278.

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Indoleamine 2,3-dioxygenase (IDO) is an enzyme that degrades an essential amino acid, tryptophan, and plays a role in inhibiting the proliferation of T cells and intracellular pathogens. Inhibiting IDO in mice leads to fetal rejection, suggesting its significance in establishing pregnancy. Toll-like receptor 3 (TLR-3) is a key component of the innate immune system that recognizes viral double-stranded RNA and triggers immune reactions by producing type I interferon. Using a human trophoblast cell culture system, we studied the effect of TLR-3 ligation on IDO expression and function by treating trophoblasts with polyinosinic-polycytidylic acid [poly(I:C)] (a synthetic double stranded RNA, which mimics viral RNA). Real-time PCR and Western blot analysis revealed that IDO mRNA and protein expression was significantly induced by poly(I:C). The activity of IDO was also increased by poly(I:C) given that the l-kynurenine concentrations were elevated in conditioned media. Conditioned media from poly(I:C)-treated trophoblasts were found to inhibit the proliferation of human T cells significantly. Poly(I:C) was also shown to induce interferon (IFN)-β mRNA expression in trophoblasts. Recombinant human IFN-β increased IDO mRNA expression in trophoblasts more rapidly than poly(I:C). Pretreating with neutralizing antibody against IFN-β significantly suppressed IDO induction by poly(I:C). Collectively we have demonstrated that ligation of TLR-3 by poly(I:C) induces IDO expression in human first-trimester trophoblasts via an IFN-β-dependent pathway. These findings suggest that upon viral infection, trophoblasts induce IDO and in turn contribute to antimicrobial activity and maintenance of fetomaternal tolerance.
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Rodriguez-Martinez, S. "Expression of CRAMP via PGN-TLR-2 and of -defensin-3 via CpG-ODN-TLR-9 in corneal fibroblasts." British Journal of Ophthalmology 90, no. 3 (March 1, 2006): 378–82. http://dx.doi.org/10.1136/bjo.2005.082289.

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Moradi, Maryam, Alireza Tabibzadeh, Davod Javanmard, Saied Ghorbani, Farah Bokharaei-Salim, Hosein Keivani, Mohammad Khazeni, and Seyed Hamid Reza Monavari. "Assessment of Key Elements in the Innate Immunity System Among Patients with HIV, HCV, and Coinfections of HIV/HCV." Current HIV Research 18, no. 3 (June 12, 2020): 194–200. http://dx.doi.org/10.2174/1570162x18999200325162533.

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Background: Coinfection of Hepatitis C virus (HCV) with human immunodeficiency virus (HIV) has a higher risk of mortality than HCV or HIV monoinfection. HCV and HIV infections are specified by systemic inflammation, but the inflammation process in HCV/HIV coinfection is much complicated and is not well characterized. Objective: The aim of this study was to analyze the expression of TLR-3, TLR-7, IL-10, IFN-1 (IFN-α, IFN-β), and TNF-α in HIV, HCV and HIV/HCV co-infected patients. Methods: Forty-five patients including HIV group (n=15), HCV group (n=15), HIV/HCV coinfection group (n=15) and healthy control group (n=15) participated. Peripheral blood mononuclear cells (PBMCs) were obtained. PBMC-RNA, HCV and HIV RNA were extracted from all subjects and cDNA was synthesized. The viral load analyzed by reverse transcription-quantitative PCR (RT-qPCR), and the expression levels of IFN-α, IFN-β, TLR-3, TLR-7, TNF, and IL-10 mRNA were quantified in PBMCs. Results: The levels of IFN-I, IL-10, and TNF-α were overexpressed in all patients’ groups (P<0.05), TLR-7 was upregulated in all groups, but this upregulation was not statistically significant (p>0.05). TLR-3 showed a decrease in all patient groups (P<0.05). The statistical analysis demonstrated that TLR-3 has a negative correlation with HIV load, whereas other genes positively correlated with HIV load. In addition, TLR-3, TNF-α, and IFN-I were negatively correlated with HCV load, whereas TLR-7 and IL-10 s were positively correlated with HCV load. Conclusion: Our results showed a significant relationship between the expression level of innate immunity genes and inflammation in HCV, HIV, and HIV/HCV coinfected patients.
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Sharma, Neel Kamal, Kaushal Sharma, Amod Gupta, Sudesh Prabhakar, Ramandeep Singh, Pawan Kumar Gupta, and Akshay Anand. "Does toll-like receptor-3 (TLR-3) have any role in Indian AMD phenotype?" Molecular and Cellular Biochemistry 393, no. 1-2 (March 30, 2014): 1–8. http://dx.doi.org/10.1007/s11010-014-2040-4.

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Firdaus, Rushna, Aritra Biswas, Kallol Saha, Anirban Mukherjee, Falguni Pal, Sujit Chaudhuri, Alok Chandra, Asokananda Konar, and Provash Chandra Sadhukhan. "Modulation of TLR 3, 7 and 8 Expressions in HCV Genotype 3 Infected Individuals: Potential Correlations of Pathogenesis and Spontaneous Clearance." BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/491064.

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Background. Hepatitis C virus is the major cause of chronic hepatitis worldwide which finally leads to the development of hepatocellular carcinoma. Toll like receptors (TLRs) play an important role in the course of many viral infections, but the role of TLRs in HCV pathogenesis has not been well elucidated so far.Objective. The aim of this study was to analyse the mRNA expression of TLRs 3, 7, and 8 in different stages of HCV infection including chronic, cirrhosis, interferon treated resolved, and relapsed cases.Methodology. Total RNA from whole blood was extracted and mRNA expression of TLRs 3, 7, and 8 genes was analyzed by quantitative real-time RT-PCR usingβ-Actin gene as an internal control.Results. This study consisted of 100 HCV infected individuals and twenty healthy controls. TLR 3 expression was found to be significantly elevated in individuals who had spontaneously cleared the virus(p<0.001), whereas TLR 7 was found to be 3.26 times more elevated in patients with cirrhosis of liver. In IFN induced individuals, TLR 8 expression levels were found to be 2.28-fold elevated as compared to control population.Conclusion. TLRs 3, 7, and 8 are prime biomarker candidates for HCV infection mRNA expression analysis which might improve current therapeutic approaches.
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Goktas, Emine Firat, Cemal Bulut, Mustafa Tugrul Goktas, Erdem Kamil Ozer, Ragip Ozgur Karaca, Sami Kinikli, Ali Pekcan Demiroz, and Atilla Bozkurt. "Investigation of 1377C/T polymorphism of the Toll-like receptor 3 among patients with chronic hepatitis B." Canadian Journal of Microbiology 62, no. 7 (July 2016): 617–22. http://dx.doi.org/10.1139/cjm-2016-0129.

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The immunopathogenesis of chronic hepatitis B (CHB) has not been clarified yet. Toll-like receptors (TLR) are a receptor family that initiates immunity with exogenous–endogenous ligands and plays a role in the pathogenesis of infections. In this study, we aimed to investigate the frequency of TLR 3 1377C/T (rs3775290) polymorphism and its role in patients with CHB. We included 50 healthy individuals as control group and 73 active and 43 inactive hepatitis B patients. All DNA samples were isolated from blood samples. For the detection of TLR 3 1377C/T single-nucleotide polymorphism, restriction fragment length polymorphism was used. A statistically significant difference was determined in Hepatitis B virus (HBV) DNA levels of CHB patients with the CC, CT, and TT genotypes (p = 0.013). The highest levels of HBV DNA were detected in individuals with TT genotypes. Additionally, the frequency of CC genotype was higher in the active CHB patients compared with that of the inactive CHB patients (p = 0.044). No statistically significant difference in TLR 3 1377C/T polymorphism was detected between healthy controls and the hepatitis B patients (p = 0.342). In conclusion, HBV DNA level was higher in the individuals with TT genotype, and CC genotype was more frequent in the active CHB patients. These results suggest a possible association between CHB and TLR 3 gene (1377C/T) polymorphism.
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Kamilov, B., M. Yuldashov, R. Khakimova, and M. Ibodova. "Age and growth of two bream species in the Tudakul reservoir of Uzbekistan." E3S Web of Conferences 244 (2021): 02041. http://dx.doi.org/10.1051/e3sconf/202124402041.

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The study was carried out in 2014-2018 at the Tudakul reservoir, Uzbekistan. Samples included 278 European bream (Abramis brama), and 83 Amur white bream (Parabramis pekinensis). The age, total length and weight of the fish varied from 1 to 5 years, from 14 to 50 cm, from 30 to 1,405 g for the European bream and from 1 to 6 years, from 24 to 53.5 cm and 105 – 2,138 g for the white Amur bream and European bream, respectively. The relationship between total length (TL) and weight (W) is described by the equation W = 0.005 * TL3.2555 (r = 0.98) for European bream and W = 0.005 * TL3.201 (r = 0.96) for white Amur bream. Recovered average growth rate of European bream: TL1 - 13.5 cm; TL2 - 28.1 cm, TL3 - 37.95 cm, TL4 - 42.6 cm, TL5 - 48.6 cm.The average height of the Amur white bream: TL1 - 12.6 cm, TL2 - 23.3 cm, TL3 - 31.5 cm, TL4 - 37.9 cm, TL5 - 41.7 cm, TL6 - 44.2 cm. Lee’s phenomenon did not appear. All yearling fish were juvenile. In 2-year-old fish of both sexes of both species, the gonads were at stage II. Males and females of both species reached their first maturity at 3-4 years of age, when the total body length of the European bream was 30–32 cm, and the Amur white bream was 34–35 cm.
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Patel, Meeta, Pankaj Kumar, Hemen Das, Abidali Dadawala, H. Chauhan, B. Chandel, N. Shah, and H. Kher. "Evaluation of the constitutive expression levels of ch-TLR 3, ch-TLR 4, ch-TLR 15 and ch-TLR 21 genes in the Peripheral Blood Mononuclear Cells of native Indian poultry breeds, Aseel and Kadaknath." Veterinary World 6, no. 8 (2013): 568. http://dx.doi.org/10.5455/vetworld.2013.568-572.

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Scagnolari, Carolina, Fabio Midulla, Alessandra Pierangeli, Corrado Moretti, Enea Bonci, Rosaria Berardi, Daniela De Angelis, et al. "Gene Expression of Nucleic Acid-Sensing Pattern Recognition Receptors in Children Hospitalized for Respiratory Syncytial Virus-Associated Acute Bronchiolitis." Clinical and Vaccine Immunology 16, no. 6 (April 22, 2009): 816–23. http://dx.doi.org/10.1128/cvi.00445-08.

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ABSTRACT Given the critical role of pattern recognition receptors (PRRs) in acid nucleic recognition in the initiation of innate immunity and the orchestration of adaptive immunity, the aim of this study was to determine whether any heterogeneity of PRR expression in the airway tracts of infants with respiratory syncytial virus (RSV) infection might explain the broad clinical spectrum of RSV-associated bronchiolitis in infants. For this purpose, the levels of melanoma differentiation-associated protein-5 (MDA-5), retinoic acid inducible gene-1 (RIG-1), and Toll-like receptor 3 (TLR-3), TLR-7, TLR-8, and TLR-9 mRNAs were evaluated, using TaqMan quantitative reverse transcription-PCR, in cells from nasopharyngeal washes collected from 157 infants suffering from acute bronchiolitis whether or not they were associated with respiratory viruses. High interindividual variability was observed in both virus-positive and -negative infants; however, the relative gene expression levels of MDA-5, RIG-1, TLR-7, and TLR-8 were significantly higher in the virus-infected group, whereas the expression levels of TLR-3 and TLR-9 were not significantly different. The differences in the gene expression of MDA-5, RIG-1, TLR-7, and TLR-8 were more evident in infants with RSV infection than in those with bocavirus or rhinovirus infection. In RSV-infected infants, PRR-mRNA levels also were analyzed in relation to interferon protein levels, viral load, clinical severity, days of hospitalization, age, and body weight. A significant positive correlation was observed only between RSV viral load and RIG-1 mRNA levels. These findings provide the first direct evidence that, in infants with respiratory virus-associated bronchiolitis, especially RSV, there are substantial changes in PRR gene expression; this likely is an important determinant of the clinical outcome of bronchiolitis.
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Klettner, Alexa, and Johann Roider. "Retinal Pigment Epithelium Expressed Toll-like Receptors and Their Potential Role in Age-Related Macular Degeneration." International Journal of Molecular Sciences 22, no. 16 (August 4, 2021): 8387. http://dx.doi.org/10.3390/ijms22168387.

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(1) Background: Inflammation is a major pathomechanism in the development and progression of age-related macular degeneration (AMD). The retinal pigment epithelium (RPE) may contribute to retinal inflammation via activation of its Toll-like receptors (TLR). TLR are pattern recognition receptors that detect the pathogen- or danger-associated molecular pattern. The involvement of TLR activation in AMD is so far not understood. (2) Methods: We performed a systematic literature research, consulting the National Library of Medicine (PubMed). (3) Results: We identified 106 studies, of which 54 were included in this review. Based on these studies, the current status of TLR in AMD, the effects of TLR in RPE activation and of the interaction of TLR activated RPE with monocytic cells are given, and the potential of TLR activation in RPE as part of the AMD development is discussed. (4) Conclusion: The activation of TLR2, -3, and -4 induces a profound pro-inflammatory response in the RPE that may contribute to (long-term) inflammation by induction of pro-inflammatory cytokines, reducing RPE function and causing RPE cell degeneration, thereby potentially constantly providing new TLR ligands, which could perpetuate and, in the long run, exacerbate the inflammatory response, which may contribute to AMD development. Furthermore, the combined activation of RPE and microglia may exacerbate neurotoxic effects.
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Whitmore, Mark M., Amaya Iparraguirre, Lindsey Kubelka, Wolfgang Weninger, Tsonwin Hai, and Bryan R. G. Williams. "Negative Regulation of TLR-Signaling Pathways by Activating Transcription Factor-3." Journal of Immunology 179, no. 6 (September 4, 2007): 3622–30. http://dx.doi.org/10.4049/jimmunol.179.6.3622.

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Chung, C. S., Y. Chen, P. Grutkoski, and A. Ayala. "BLOCKADE OF TLR-NFkB SIGNALING DOWNREGULATE SOCS-3 EXPRESSION DURING SEPSIS." Shock 21 (June 2004): 80. http://dx.doi.org/10.1097/00024382-200406002-00237.

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Mishra, Om P., Ravindra Kumar, Gopeshwar Narayan, Pradeep Srivastava, Abhishek Abhinay, Rajniti Prasad, Ankur Singh, and Vineeta V. Batra. "Toll-like receptor 3 (TLR-3), TLR-4 and CD80 expression in peripheral blood mononuclear cells and urinary CD80 levels in children with idiopathic nephrotic syndrome." Pediatric Nephrology 32, no. 8 (February 16, 2017): 1355–61. http://dx.doi.org/10.1007/s00467-017-3613-8.

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Zhou, Rongbin, Haiming Wei, Rui Sun, Jian Zhang, and Zhigang Tian. "NKG2D recognition mediates Toll-like receptor 3 signaling-induced breakdown of epithelial homeostasis in the small intestines of mice." Proceedings of the National Academy of Sciences 104, no. 18 (April 26, 2007): 7512–15. http://dx.doi.org/10.1073/pnas.0700822104.

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Toll-like receptors (TLRs) and NK receptors are the two most important receptor families in innate immunity. Although it has been observed that TLR signaling can induce or up-regulate the expression of the ligands for stimulatory NK receptors on monocytes or muscle cells, there is not yet a report indicating whether TLR signaling can break down self-tolerance through NK receptors. The present work reports that TLR3 signaling by polyinosinic–polycytidylic acid stimulation induces intestinal epithelial cells (IECs) to express retinoic acid early inducible-1 (a ligand for NKG2D) and to induce NKG2D expression on CD8αα intestinal intraepithelial lymphocytes by IL-15 derived from TLR3-activated IECs. The blockade of interaction between NKG2D and Rae1 inhibits the cytotoxicity of intraepithelial lymphocytes against IECs in a cell–cell contact-dependent manner and therefore alleviates polyinosinic–polycytidylic acid-induced epithelial destruction and acute mucosal injury of small intestine. These results demonstrate that TLR signaling induces tissue injury through the NKG2D pathway, suggesting that TLR signaling may break down self-tolerance through induction of abnormal expression of ligands for stimulatory NK receptors.
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Traumann, Ada, Teele Peets, Inga Dabolina, and Eva Lapkovska. "Analysis of 3-D body measurements to determine trousers sizes of military combat clothing." Textile & leather review 2, no. 1 (March 11, 2019): 6–14. http://dx.doi.org/10.31881/tlr.2019.2.

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The aim of this paper was to analyse several measurements of soldiers to provide a reference for trousers sizes of military combat clothing. For sizing and fitting of military clothing, information on the body measurements of the user population is a precondition. More than 400 soldiers in the Estonian and Latvian Defence Forces as well as the military personnel were measured using Human Solution 3-D scanner. It focused on collating basic human body measurement data for the revision of size charts by STANAG 2335. Fit and comfort of trousers mainly relate to the following measurements: waist girth, leg inseam, leg length, and waistband. Present parameters play a significant role in the quality of trousers to ensure the wearer’s mobility in all situations particularly concerning the activities of soldiers. Correlating measurements and existing sizing systems are made to offer recommendations for manufacturers. In addition, this paper helps to provide sizing and fitting criteria of military combat clothing to STANREC document compiled by NATO RTO HFM-266 Group.
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Moreno-Eutimio, Mario Adan, Raul Aragon-Franco, Constantino Lopez-Macias, Alejandro J. Silva, and Horacio Astudillo. "Toll-like receptor 7 and 9 (TLR 7 and TLR 9) expression in biopsies of in situ cervical cancer." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e15584-e15584. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e15584.

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e15584 Background: In order to analyze the expression of TLR 7 and TLR 9 in cervix biopsies, we evaluated the expression of these TLRs in cervical carcinoma in situ tissue and peritumoral inflammatory tissue biopsies by immunohistochemistry. Methods: We reviewed 276 uterine cervix biopsies of Clinical Specialties Women's Health Directorate of the Ministry of National Defense (between 2009-2010); the biopsies have the following histopathological diagnosis: 124 CIN I, 68 CIN II, 34 CIN III, 21 invasive cancer and 29 cancer in situ. Results: It was observed that peritumoral inflammatory tissue receptor was expressed positively in 89.6% in cervical cancer tissue in situ, the receptor was expressed positively in 68.9% and the negative expression was 31.1%, proving that in the peritumoral inflammatory tissue compared with in situ cervical cancer was increased expression of TLR 7. In the case of the expression of TLR 9, peritumoral inflammatory tissue, expressed positively in 24 samples and 5 samples were negative expression in the tissue in situ cervical cancer samples identified 20 positive and 9 negative samples. By analyzing the intensity of the expression of TLR 7 in cervical cancer tissue in situ, we found 16 samples with focal positive (+), 3 samples with diffuse positive (+ +) and 1 sample with positive (+ + + ), while in peritumoral inflammatory tissue found 13 samples with focal positive (+), 10 samples with diffuse positive (+ +) and 3 samples with positive results (+++). By analyzing the intensity of the expression of TLR 9 in cervical cancer tissue in situ, we found 14 samples with focal positive (+), 5 samples with diffuse positive (+ +) and 1 sample with positive (+), in contrast to the peritumoral inflammatory tissue was found 7 samples with focal positive (+), 13 samples tested positive diffuse (+ +) and 4 samples with positive results (+++). Conclusions: These results show that no significant difference between the expression of TLR 7 () and TLR 9 () in the peritumoral inflammatory tissue and tissue in situ cervical cancer found a decrease in the expression of TLR 7 and TLR 9 in tissue in situ cervical cancer compared with the expression in the peritumoral tissue inflammation.
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Panneton, Jean M., Jean Bismuth, Bruce H. Gray, and Andrew Holden. "Three-Year Follow-up of Patients With Iliac Occlusive Disease Treated With the Viabahn Balloon- Expandable Endoprosthesis." Journal of Endovascular Therapy 27, no. 5 (April 24, 2020): 728–36. http://dx.doi.org/10.1177/1526602820920569.

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Purpose: To assess the midterm safety and effectiveness of the Gore Viabahn Balloon-Expandable Endoprosthesis (VBX Stent-Graft) in the treatment of patients with de novo or restenotic aortoiliac lesions. Materials and Methods: The prospective, multicenter, nonrandomized, single-arm VBX FLEX clinical study ( ClinicalTrials.gov identifier: NCT02080871) evaluated 134 patients (mean age 66±9.5 years; 79 men) up to 3 years after treatment with the VBX Stent-Graft. A total of 213 lesions were treated with 234 stent-grafts. The primary safety endpoint was a composite of major adverse events (MAEs), which were evaluated through 30 days and 9 months. Secondary outcomes collected through 3 years included freedom from target lesion revascularization (TLR), target vessel revascularization (TVR), clinically-driven TLR (CD-TLR), and CD-TVR as well as Rutherford category, resting ankle-brachial index (ABI), and functional status. A univariate analysis determined any correlation between baseline variables and TLR. Results: The observed composite percentage of MAEs was 2.3%, well below the 17% performance goal (p<0.001). Of the 134 patients in the per protocol analysis, 107 (80%) completed the study. The 1-year Kaplan-Meier estimate of primary patency was 94.5% and primary assisted patency was 99.0%. The estimate of freedom from TLR per-lesion/vessel was 97.6% at 9 months and 91.2% at 3 years. The 9-month estimate of freedom from CD-TLR was 98.6% and the 3-year estimate was 98.1%. The 3-year mean resting ABI was 0.93±0.19, an improvement of 0.17±0.26 from baseline (p<0.001). At 3 years, 82 patients (92.1%) improved ≥1 Rutherford category from baseline, and 77 patients (86.5%) maintained or improved upon their baseline functional status. Conclusion: The VBX Stent-Graft is a robust and durable treatment option for aortoiliac occlusive disease as evidenced by the sustained 3-year safety and effectiveness outcomes.
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Epaulard, O., L. Adam, R. Le Grand, and F. Martinon. "TLR-3 and TLR-7/8 ligands indirectly activate Langerhans cells when intradermally injected by triggering the recruitment of inflammatory cells." Retrovirology 9, Suppl 2 (2012): P7. http://dx.doi.org/10.1186/1742-4690-9-s2-p7.

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Litak, Jakub, Cezary Grochowski, Joanna Litak, Ida Osuchowska, Krzysztof Gosik, Elżbieta Radzikowska, Piotr Kamieniak, and Jacek Rolinski. "TLR-4 Signaling vs. Immune Checkpoints, miRNAs Molecules, Cancer Stem Cells, and Wingless-Signaling Interplay in Glioblastoma Multiforme—Future Perspectives." International Journal of Molecular Sciences 21, no. 9 (April 28, 2020): 3114. http://dx.doi.org/10.3390/ijms21093114.

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Toll-like-receptor (TLR) family members were detected in the central nervous system (CNS). TLR occurrence was noticed and widely described in glioblastomamultiforme (GBM) cells. After ligand attachment, TLR-4 reorients domains and dimerizes, activates an intracellular cascade, and promotes further cytoplasmatic signaling. There is evidence pointing at a strong relation between TLR-4 signaling and micro ribonucleic acid (miRNA) expression. The TLR-4/miRNA interplay changes typical signaling and encourages them to be a target for modern immunotherapy. TLR-4 agonists initiate signaling and promote programmed death ligand-1 (PD-1L) expression. Most of those molecules are intensively expressed in the GBM microenvironment, resulting in the autocrine induction of regional immunosuppression. Another potential target for immunotreatment is connected with limited TLR-4 signaling that promotes Wnt/DKK-3/claudine-5 signaling, resulting in a limitation of GBM invasiveness. Interestingly, TLR-4 expression results in bordering proliferative trends in cancer stem cells (CSC) and GBM. All of these potential targets could bring new hope for patients suffering from this incurable disease. Clinical trials concerning TLR-4 signaling inhibition/promotion in many cancers are recruiting patients. There is still a lot to do in the field of GBM immunotherapy.
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Behm, Christian, Alice Blufstein, Johannes Gahn, Barbara Kubin, Andreas Moritz, Xiaohui Rausch-Fan, and Oleh Andrukhov. "Continuing Effect of Cytokines and Toll-Like Receptor Agonists on Indoleamine-2,3-Dioxygenase-1 in Human Periodontal Ligament Stem/Stromal Cells." Cells 9, no. 12 (December 16, 2020): 2696. http://dx.doi.org/10.3390/cells9122696.

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Transplanted mesenchymal stem/stromal cells (MSCs) are a promising and innovative approach in regenerative medicine. Their regenerative potential is partly based upon their immunomodulatory activities. One of the most investigated immunomediators in MSCs, such as in periodontal ligament-derived MSCs (hPDLSCs), is indoleamine-2,3-dioxygenase-1 (IDO-1) which is upregulated by inflammatory stimuli, like cytokines. However, there are no data concerning continuing IDO-1 expression in hPDLSCs after the removal of inflammatory stimuli, such as cytokines and toll-like receptor (TLR) agonist-2 and TLR-3. Hence, primary hPDLSCs were stimulated with interleukin (IL)-1β, tumor necrosis factor (TNF)-α, interferon (IFN)-γ, TLR-2 agonist Pam3CSK4 or TLR-3 agonist Poly I/C. IDO-1 gene and protein expression and its enzymatic activity were measured up to five days after removing any stimuli. IL-1β- and TNF-α-induced IDO-1 expression and enzymatic activity decreased in a time-dependent manner after cessation of stimulation. IFN-γ caused a long-lasting effect on IDO-1 up to five days after removing IFN-γ. Both, TLR-2 and TLR-3 agonists induced a significant increase in IDO-1 gene expression, but only TLR-3 agonist induced significantly higher IDO-1 protein expression and enzymatic activity in conditioned media (CM). IDO-1 activity of Poly I/C- and Pam3CSK4-treated hPDLSCs was higher at one day after removal of stimuli than immediately after stimulation and declined to basal levels after five days. Among all tested stimuli, only IFN-γ was able to induce long-lasting IDO-1 expression and activity in hPDLSCs. The high plasticity of IDO-1 expression and its enzymatic activity in hPDLSCs due to the variable cytokine and virulence factor milieu and the temporal-dependent responsiveness of hPDLSCs may cause a highly dynamic potential of hPDLSCs to modulate immune responses in periodontal tissues.
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Farina, Roberto, Anna Simonelli, Andrea Baraldi, Mattia Pramstraller, Luigi Minenna, Luca Toselli, Elisa Maietti, and Leonardo Trombelli. "Tooth loss in complying and non-complying periodontitis patients with different periodontal risk levels during supportive periodontal care." Clinical Oral Investigations 25, no. 10 (March 24, 2021): 5897–906. http://dx.doi.org/10.1007/s00784-021-03895-8.

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Abstract Objectives To evaluate yearly tooth loss rate (TLR) in periodontitis patients with different periodontal risk levels who had complied or not complied with supportive periodontal care (SPC). Materials and methods Data from 168 periodontitis patients enrolled in a SPC program based on a 3-month suggested recall interval for at least 3.5 years were analyzed. For patients with a mean recall interval within 2–4 months (“compliers”) or > 4 months (“non-compliers”) with different PerioRisk levels (Trombelli et al. 2009), TLR (irrespective of the cause for tooth loss) was calculated. TLR values were considered in relation to meaningful TLR benchmarks from the literature for periodontitis patients either under SPC (0.15 teeth/year; positive benchmark) or irregularly complying with SPC (0.36 teeth/year; negative benchmark). Results In both compliers and non-compliers, TLR was significantly below or similar to the positive benchmark in PerioRisk level 3 (0.08 and 0.03 teeth/year, respectively) and PerioRisk level 4 (0.12 and 0.18 teeth/year, respectively). Although marked and clinically relevant in non-compliers, the difference between TLR of compliers (0.32 teeth/year) and non-compliers (0.52 teeth/year) with PerioRisk level 5 and the negative benchmark was not significant. Conclusion A SPC protocol based on a 3- to 6-month recall interval may effectively limit long-term tooth loss in periodontitis patients with PerioRisk levels 3 and 4. A fully complied 3-month SPC protocol seems ineffective when applied to PerioRisk level 5 patients. Clinical relevance PerioRisk seems to represent a valid tool to inform the SPC recall interval as well as the intensity of active treatment prior to SPC enrollment.
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Higgs, Rowan, Paul Cormican, Sarah Cahalane, Brenda Allan, Andrew T. Lloyd, Kieran Meade, Tharappel James, David J. Lynn, Lorne A. Babiuk, and Cliona O'Farrelly. "Induction of a Novel Chicken Toll-Like Receptor following Salmonella enterica Serovar Typhimurium Infection." Infection and Immunity 74, no. 3 (March 2006): 1692–98. http://dx.doi.org/10.1128/iai.74.3.1692-1698.2006.

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ABSTRACT Toll-like receptors (TLRs) are a group of highly conserved molecules that initiate the innate immune response to pathogens by recognizing structural motifs expressed by microbes. We have identified a novel TLR, TLR15, by bioinformatic analysis of the chicken genome, which is distinct from any known vertebrate TLR and thus appears to be avian specific. The gene for TLR15 was sequenced and is found on chromosome 3, and it has archetypal TIR and transmembrane domains and a distinctive arrangement of extracellular leucine-rich regions. mRNA for TLR15 was detected in the spleen, bursa, and bone marrow of healthy chickens, suggesting a role for this novel receptor in constitutive host defense. Following in vivo Salmonella enterica serovar Typhimurium infection, quantitative real-time PCR demonstrated significant upregulation of TLR15 in the cecum of infected chickens. Interestingly, similar induction of TLR2 expression following infection was also observed. In vitro studies revealed TLR15 upregulation in chicken embryonic fibroblasts stimulated with heat-killed S. enterica serovar Typhimurium. Collectively, these results suggest a role for the TLR in avian defense against bacterial infection. We hypothesize that TLR15 may represent an avian-specific TLR that has been either retained in chicken and lost in other taxa or gained in the chicken.
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Ziegler, Patrick, Steffen Boettcher, Guido Garavaglia, and Markus G. Manz. "TLR4-Agonist Stimulated Human Multipotent Mesenchymal Stromal Cells Enhance Both Hematopoietic Progenitors and Myeloid Differentiation." Blood 112, no. 11 (November 16, 2008): 1366. http://dx.doi.org/10.1182/blood.v112.11.1366.1366.

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Abstract Human mesenchymal stromal cells (MSCs) can replicate as undifferentiated cells in vitro and are capable of differentiating into multiple mesenchymal tissues. In the bone marrow, MSCs are thought to contribute to nurturing stroma involved in maintaining and modulating hematopoiesis. Toll-like receptors (TLRs) function as receptors for different conserved pathogen associated products as well as certain host derived molecules. TLRs are expressed in several hematopoietic and non-hematopoietic cells, and their activation plays a key role in innate and adaptive immune responses to infectious agents, as well as in the development of pathologic conditions like autoimmune disease. In inflammatory conditions like sepsis, cytokines like G-CSF are elevated in serum, CD34+ cells increase in circulation, and bone marrow myelopoiesis is enhanced. We hypothesized that MSCs express TLRs and are capable to respond to TLR agonists by changing their cytokine expression pattern in order to more efficiently support hematopoiesis according to respective needs. In vitro cultured bone marrow MSCs were analyzed for mRNA expression of TLRs. TLR 1, 3, 4, 5, 6, and 9 expression, but not TLR 2, 7, 8, and 10 expression was detectable. Compared to human conventional and plasmacytoid blood dendritic cells, MSCs expressed TLR-3 and TLR-4 at levels up to 2 log higher than did conventional DCs, while TLR 9 expression was low. Upon in vitro stimulation with TLR-4 agonists, mRNA transcripts of flt3-ligand and thrombopoietin increased, and MSCs secreted high amounts of G-CSF, GM-CSF, and M-CSF, whereas stimulation with TLR-9 agonists did not lead to changes in cytokine levels measured in supernatants. TLR-4 stimulated MSC conditioned media enhanced myeloid colony formation from human CD34+ cells about 2.5× fold compared to non-stimulated MSC conditioned media. Furthermore, in co-culture assays of MSCs with CD34+ cells, TLR-4 stimulated MSCs were capable to retain 8 fold more CD34+ cells in divisions 0–3 and maintained overall 2 fold higher numbers of CD34+ cells. In secondary colony formation assays, CD34+ cells from TLR-4 stimulated MSC co-cultures produced about 2.5 fold more myeloid colonies, with some being CFU-GEMM. Moreover, hematopoietic cells taken from TLR-4 stimulated MSC co-cultures were able to engraft conditioned newborn Rag 2−/− gc−/− mice and differentiated into B, T, and myeloid cells, while CD34+ cells from co-cultures of non-stimulated MSCs did not engraft. These findings thus suggest a regulatory mechanism how, e.g. in gram-negative infection, inflammatory signals are translated via stromal cells into sustained early hematopoiesis and myeloid differentiation to efficiently meet the requests of an ongoing innate immune response.
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ENEVOLD, CHRISTIAN, TIMOTHY R. D. RADSTAKE, MARIEKE J. H. COENEN, JAAP FRANSEN, ERIK J. M. TOONEN, KLAUS BENDTZEN, and PIET L. C. M. van RIEL. "Multiplex Screening of 22 Single-Nucleotide Polymorphisms in 7 Toll-like Receptors: An Association Study in Rheumatoid Arthritis." Journal of Rheumatology 37, no. 5 (March 1, 2010): 905–10. http://dx.doi.org/10.3899/jrheum.090775.

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Objective.Toll-like receptors (TLR) have been implicated in the pathogenesis of arthritis. We investigated the role of functional variants of TLR in the disease phenotype and severity of rheumatoid arthritis (RA).Methods.All patients from a longterm observational inception cohort (n = 319) were genotyped for 22 single-nucleotide polymorphisms (SNP) in TLR2, 3, 4, 5, 7, 8, and 9 using multiplex assays. Clinical characteristics including sex, age at disease onset, rheumatoid factor (RF), and shared epitope positivity and disease activity score and radiological progression were taken into account. Genotypes were analyzed for association with Disease Activity Scores (DAS28) and joint damage (Rau scores) at 3 and 6 years.Results.After Bonferroni correction, there was a moderate association between RF positivity and TLR8-rs5741883. No other TLR variant was significantly associated with any RA clinical characteristics.Conclusion.Using a large inception cohort and strict statistical evaluation, we could not identify an association between functional TLR variants and RA phenotype and disease severity. This suggests the functional TLR variants do not play a major role in RA phenotype and disease severity.
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Li, Xiaofeng, Tao Xu, Yarui Wang, Cheng Huang, and Jun Li. "Toll-like receptor (TLR)-3: a potent driving force behind rheumatoid arthritis." Clinical Rheumatology 33, no. 2 (November 21, 2013): 291–92. http://dx.doi.org/10.1007/s10067-013-2418-9.

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Yamamura, Yuriko, Shin Morizane, and Keiji Iwatsuki. "Terminal differentiation of keratinocytes enhances TLR 3 expression and anti-viral activity." Journal of Dermatological Science 84, no. 1 (October 2016): e165. http://dx.doi.org/10.1016/j.jdermsci.2016.08.488.

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Xu, Dakang, Bandar Suliman, Anthony J. Sadler, and Bryan R. G. Williams. "PL2-3 Negative regulation of TLR-mediated NF-κB activation by PLZF." Cytokine 52, no. 1-2 (October 2010): 36. http://dx.doi.org/10.1016/j.cyto.2010.07.164.

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Cramer, J. P., B. Lepenies, C. Hölscher, M. Freudenberg, G. D. Burchard, and T. Jacobs. "O60 TLR-cascade in malaria: role in antiparasitic clearance." International Journal of Antimicrobial Agents 29 (March 2007): S14—S15. http://dx.doi.org/10.1016/s0924-8579(07)70049-3.

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Ishii, Ken J., Fumihiko Takeshita, Ihsan Gursel, Mayda Gursel, Jacqueline Conover, Andre Nussenzweig, and Dennis M. Klinman. "Potential Role of Phosphatidylinositol 3 Kinase, rather than DNA-dependent Protein Kinase, in CpG DNA–induced Immune Activation." Journal of Experimental Medicine 196, no. 2 (July 8, 2002): 269–74. http://dx.doi.org/10.1084/jem.20020773.

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Unmethylated CpG motifs present in bacterial DNA stimulate a strong innate immune response. There is evidence that DNA-dependent protein kinase (DNA-PK) mediates CpG signaling. Specifically, wortmannin (an inhibitor of phosphatidylinositol 3 kinase [PI3]-kinases including DNA-PK) interferes with CpG-dependent cell activation, and DNA-PK knockout (KO) mice fail to respond to CpG stimulation. Current studies establish that wortmannin actually inhibits the uptake and colocalization of CpG DNA with toll-like receptor (TLR)-9 in endocytic vesicles, thereby preventing CpG-induced activation of the NF-κB signaling cascade. We find that DNA-PK is not involved in this process, since three strains of DNA-PK KO mice responded normally to CpG DNA. These results support a model in which CpG signaling is mediated through TLR-9 but not DNA-PK, and suggest that wortmannin-sensitive member(s) of the PI3-kinase family play a critical role in shuttling CpG DNA to TLR-9.
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Kim, Dhohyung, and Stefan Niewiesk. "Synergistic induction of interferon α through TLR-3 and TLR-9 agonists stimulates immune responses against measles virus in neonatal cotton rats." Vaccine 32, no. 2 (January 2014): 265–70. http://dx.doi.org/10.1016/j.vaccine.2013.11.013.

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Butt, Aisha Qasim, Suaad Ahmed, Ashwini Maratha, and Sinéad M. Miggin. "14-3-3ϵ and 14-3-3σ Inhibit Toll-like Receptor (TLR)-mediated Proinflammatory Cytokine Induction." Journal of Biological Chemistry 287, no. 46 (September 14, 2012): 38665–79. http://dx.doi.org/10.1074/jbc.m112.367490.

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