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Artykuły w czasopismach na temat „TLR- 3”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 1 lutego 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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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

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4

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 seroconv

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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.

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López-Haber, Cynthia, Roni Levin-Konigsberg, Yueyao Zhu, Jing Bi-Karchin, Tamas Balla, Sergio Grinstein, Michael S. Marks та 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, № 45 (27 жовтня 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 t

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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 monocyt

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10

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 monocyt

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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(

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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

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13

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

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15

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

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16

Collins, Patricia E., Domenico Somma, David Kerrigan, Felicity Herrington, Karen Keeshan, Robert J. B. Nibbs та 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, № 51 (26 листопада 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 nuc

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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.Objec

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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

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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 heal

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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

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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

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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

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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,

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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

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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 NKG

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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 gi

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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 re

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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), w

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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 promot

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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-

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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 v

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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

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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 infectiou

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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

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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 та Bryan R. G. Williams. "PL2-3 Negative regulation of TLR-mediated NF-κB activation by PLZF". Cytokine 52, № 1-2 (жовтень 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 N

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Kim, Dhohyung, та 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, № 2 (січень 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 та Sinéad M. Miggin. "14-3-3ϵ and 14-3-3σ Inhibit Toll-like Receptor (TLR)-mediated Proinflammatory Cytokine Induction". Journal of Biological Chemistry 287, № 46 (14 вересня 2012): 38665–79. http://dx.doi.org/10.1074/jbc.m112.367490.

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