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Artykuły w czasopismach na temat "Toll-like receptors"
Lien, Egil, i Robin R. Ingalls. "Toll-like receptors". Critical Care Medicine 30, Suppl. (styczeń 2002): S1—S11. http://dx.doi.org/10.1097/00003246-200201001-00001.
Pełny tekst źródłaErickson, Benjamin, Kirk Sperber i William H. Frishman. "Toll-Like Receptors". Cardiology in Review 16, nr 6 (listopad 2008): 273–79. http://dx.doi.org/10.1097/crd.0b013e3181709fd8.
Pełny tekst źródłaWarren, H. Shaw. "Toll-like receptors". Critical Care Medicine 33, Suppl (grudzień 2005): S457—S459. http://dx.doi.org/10.1097/01.ccm.0000185504.39347.5d.
Pełny tekst źródłaShin, Ho. "Toll-like Receptors". British Journal of Medicine and Medical Research 3, nr 1 (10.01.2013): 58–68. http://dx.doi.org/10.9734/bjmmr/2013/2071.
Pełny tekst źródłaMuzio, Marta, i Alberto Mantovani. "Toll-like receptors". Microbes and Infection 2, nr 3 (marzec 2000): 251–55. http://dx.doi.org/10.1016/s1286-4579(00)00303-8.
Pełny tekst źródłaMoresco, Eva Marie Y., Diantha LaVine i Bruce Beutler. "Toll-like receptors". Current Biology 21, nr 13 (lipiec 2011): R488—R493. http://dx.doi.org/10.1016/j.cub.2011.05.039.
Pełny tekst źródłaBilak, H., S. Tauszig-Delamasure i J. L. Imler. "Toll and Toll-like receptors in Drosophila". Biochemical Society Transactions 31, nr 3 (1.06.2003): 648–51. http://dx.doi.org/10.1042/bst0310648.
Pełny tekst źródłaAkira, Shizuo. "Mammalian Toll-like receptors". Current Opinion in Immunology 15, nr 1 (luty 2003): 5–11. http://dx.doi.org/10.1016/s0952-7915(02)00013-4.
Pełny tekst źródłaAkira, Shizuo. "Mammalian Toll-like receptors". Current Opinion in Immunology 15, nr 2 (kwiecień 2003): 238. http://dx.doi.org/10.1016/s0952-7915(03)00005-0.
Pełny tekst źródłaModlin, Robert L. "Mammalian Toll-like receptors". Annals of Allergy, Asthma & Immunology 88, nr 6 (czerwiec 2002): 543–48. http://dx.doi.org/10.1016/s1081-1206(10)61883-2.
Pełny tekst źródłaRozprawy doktorskie na temat "Toll-like receptors"
Carrenho, Luciana Cristina de Andrade [UNESP]. "Avaliação ex vivo da expressão de TLR-2 e TLR-4 em leucócitos de equinos e sua relação com a tolerância à endotoxina". Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/92210.
Pełny tekst źródłaA endotoxemia é um importante distúrbio sistêmico que se origina da resposta do hospedeiro a um componente das bactérias Gram-negativas, o lipopolissacarídeo (LPS) ou endotoxina, que é liberado após bacteriólise ou rápida multiplicação. A ativação do sistema imune inato pelo LPS é um fator chave para o disparo da resposta inflamatória pelo hospedeiro e que acarreta a produção de mediadores inflamatórios, responsáveis pelos eventos patológicos da endotoxemia. A interação dos receptores Toll-like (TLRs) com antígenos específicos deflagram a resposta inflamatória, sendo que o receptor Toll-like-4 (TLR-4) é ativado pela ação das endotoxinas, enquanto o receptor Toll-like-2 (TLR-2) interage com uma variedade de componentes microbianos. Uma exposição prévia a baixas concentrações de LPS pode tornar os cavalos “tolerantes” a um desafio letal subsequente, acarretando uma diminuição na produção de citocinas inflamatórias por um período transitório. Pouco se sabe a respeito do mecanismo celular deste fenômeno em equinos, supondo-se o envolvimento dos receptores Toll-like semelhante ao encontrado em outras espécies. Com este estudo investigaram-se os mecanismos celulares da tolerância à endotoxina em um modelo ex vivo com sangue total. Foi demonstrado redução na síntese de citocinas pró-inflamatórias (TNF-α, IL-1 e IL-6), aumento da expressão gênica da citocina anti-inflamatória IL-10, e ausência de expressão do TGF-β, após o desafio secundário com LPS. A maior expressão dos receptores TLR-2 e -4 após o segundo estímulo de LPS demonstrou que a tolerância à endotoxina não acarreta diminuição da expressão de ambos os receptores em equinos.
Endotoxemia is an important systemic disease originated from host response to a component of Gram-negative bacteria, lipopolysaccharide (LPS) or endotoxin, which is released after bacteria death or quick replication. The innate immune recognition of LPS has a key role triggering host inflammatory answer and is due to inflammatory mediator’s synthesis, which are responsible for pathologic events of endotoxemia. Signs initiated by interaction of Toll-like receptors (TLRs) with specific products induce the inflammatory response. Toll-like receptor-4 (TLR- 4) is activated by endotoxin action while Toll-like receptor-2 (TLR-2) interacts with a range of microbial compounds. Some studies demonstrate that both can act like LPS receptors, although by independent pathways. It was demonstrated that a previous exposition to low concentrations of LPS can render horses “tolerant” to a lethal subsequent challenge with endotoxin, leading to a diminished release of inflammatory cytokines during a transient period. However, little is known about the cellular mechanisms involved in this phenomenon in horses, suspecting that there is involvement of cell surface receptors, similarly to other species. This study investigated cellular mechanisms of endotoxin tolerance in a whole blood ex vivo model, demonstrating a reduction on pro-inflammatory cytokines synthesis (TNF- α, IL-1 and IL-6), increased gene expression of anti-inflammatory cytokine IL-10 and no alteration in TGF-β expression, after a secondary stimulus with LPS. The Toll-like receptors-2 and -4 increased expression after a second stimulus with LPS showed that endotoxin tolerance does not lead to a decreased expression of both receptors in horses.
Offord, Victoria Anne. "Toll-like receptors : from sequence to structure". Thesis, Royal Veterinary College (University of London), 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669195.
Pełny tekst źródłaIrvine, Katherine Lucy. "The pharmacology of equine toll-like receptors". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608103.
Pełny tekst źródłaDessing, Mark Christianus. "Toll-like receptors and innate immunity in pneumonia". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2007. http://dare.uva.nl/document/47971.
Pełny tekst źródłaPhilbin, Victoria Jane. "Identification & characterisation of avian toll-like receptors". Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.425894.
Pełny tekst źródłaCant, Rachel. "Modulation of toll like receptors by naltrexone hydrochloride". Thesis, St George's, University of London, 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.753993.
Pełny tekst źródłaKassem, Ali. "Toll-like receptors (TLRs) and inflammatory bone modeling". Doctoral thesis, Umeå universitet, Institutionen för odontologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-110296.
Pełny tekst źródłaWeber, Alexander Norman Rainer. "Structural and functional studies of Drosophila toll and human toll-like receptors". Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615987.
Pełny tekst źródłaBraedel-Ruoff, Sibylla. "Toll-like receptors - link between innate and adaptive immunity". [S.l. : s.n.], 2007.
Znajdź pełny tekst źródłaEstévez, Medina Javier. "Toll-like receptors as modulators of intestinal barrier function". Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/400146.
Pełny tekst źródłaFunctional (irritable bowel syndrome, IBS) and inflammatory (inflammatory bowel disease, IBD) gastrointestinal disorders are characterized by an altered epithelial barrier function, with an increased permeability, and changes in the intestinal microbiota. Toll-Like Receptors (TLRs) participates in bacterial recognition within the intestine and in local neuro-immune control, thus participating in the regulation of intestinal epithelial barrier function. The objective of this work has been to characterize the implication of TLR5 and TLR7 in the regulation of colonic epithelial barrier function. For this, colonic epithelial barrier function has been studied in vitro (electrophysiology and permeability to macromolecules in a Ussing chamber system), as well as in in vivo conditions (permeability to macromolecules), after the local over-stimulation of TLR5 and TLR7 with selective agonists, flagellin and imiquimod, respectively, in rats and mice. The effects on barrier function have been studied in normal conditions, under states epithelial permeabilization with DMSO, and in conditions of inflammation -dextran sulfate sodium (DSS)-induced colitis-. In order to characterize the mechanisms of action, dynamics of tight junction (gene expression -RT-qPCR- and cellular distribution -immunohistochemistry- of tight junction proteins) and the presence of a local immune activation (gene expression of pro-inflammatory cytokines) were assessed. The results obtained indicate that the in vivo over-stimulation of colonic TLR7 improves epithelial barrier function in rats in physiological conditions, with a dose-dependent reduction in epithelial permeability to macromolecules, as assessed in Ussing chambers. However, under conditions of epithelial permeabilization with DMSO, the over-stimulation of TLR7 deteriorates barrier function, as assessed in vivo. In mice, the in vitro over-stimulation of colonic TLR7 was without effects. However, in a model of DSS-induced colitis, imiquimod reduces inflammation-induced increased epithelial permeability. Therefore, specie-specific differences seemed to exist for the barrier effects associated to the over-stimulation of colonic TLR7, leading to either protective or damaging actions on epithelial barrier function, depending upon the experimental conditions. The over-stimulation of colonic TLR5 aggravates the barrier dysfunction associated to inflammation (DSS-induced colitis) in mice, increasing the permeability to macromolecules. However, the direct addition of flagellin to the Ussing chambers did not affect epithelial barrier function, neither in physiologic conditions nor during inflammation. Regardless the conditions considered, TLR5/7-mediated modulatory actions on barrier function were not associated to changes in gene expression of the main tight junction-related proteins (claudin-2, claudin-3, occludin, tricellulin, junctional adhesion molecule 1 and Zonula Occludens 1). Moreover, no changes in the cellular distribution of tight junction proteins (claudin-2, claudin-3 y ZO-1) was observed. Likewise, TLR5/7 over-stimulation was not associated to changes in the expression of the barrier-modulating factors myosin light chain kinase and proglucagon (precursor of glucagon-like peptide 2). Finally, TLR-specific immunomodulatory effects were also observed. Over-stimulation of TLR7 revealed potential protective effects, reducing the expression of the pro-inflammatory cytokine IL12-p40. In contrast, over-stimulation of TLR5 tended to increase the expression of pro-inflammatory markers, thus suggesting pro-damaging effects. In conclusion, these results provide evidence of the importance of TLRs-dependent host-microbial interactions in the control of intestinal epithelial barrier function. Colonic TLR5 and TLR7 should be considered potential therapeutic targets for the control of barrier function and local immune responses in functional and gastrointestinal disorders, such as IBD and IBS.
Książki na temat "Toll-like receptors"
McCoy, Claire E., i Luke A. J. O’Neill, red. Toll-Like Receptors. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-541-1.
Pełny tekst źródłaMcCoy, Claire E., red. Toll-Like Receptors. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3335-8.
Pełny tekst źródłaFallarino, Francesca, Marco Gargaro i Giorgia Manni, red. Toll-Like Receptors. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3366-3.
Pełny tekst źródłaO’Neill, Luke A. J., i Elizabeth Brint, red. Toll-like Receptors in Inflammation. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/3-7643-7441-1.
Pełny tekst źródłaJ, O'Neill Luke A., i Brint Elizabeth, red. Toll-like receptors in inflammation. Basel: Birkhäuser Verlag, 2005.
Znajdź pełny tekst źródłaW, Konat Gregory, red. Signaling by toll-like receptors. Boca Raton: Taylor & Francis Group, 2008.
Znajdź pełny tekst źródłaKumar, Vijay, red. Toll-like Receptors in Health and Disease. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-06512-5.
Pełny tekst źródłaBauer, Stefan, i Gunther Hartmann, red. Toll-Like Receptors (TLRs) and Innate Immunity. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-72167-3.
Pełny tekst źródłaProf, Bauer Stefan, Hartmann Gunther 1966- i Akira S, red. Toll-like receptors (TLRs) and innate immunity. Berlin: Springer, 2008.
Znajdź pełny tekst źródłaProf, Bauer Stefan, Hartmann Gunther 1966- i Akira S, red. Toll-like receptors (TLRs) and innate immunity. Berlin: Springer, 2008.
Znajdź pełny tekst źródłaCzęści książek na temat "Toll-like receptors"
Shiu, Jessica, i Anthony A. Gaspari. "Toll-Like Receptors". W Clinical and Basic Immunodermatology, 11–34. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-29785-9_2.
Pełny tekst źródłaPugin, Jérôme. "Toll-Like Receptors". W Evolving Concepts in Sepsis and Septic Shock, 27–44. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1581-4_3.
Pełny tekst źródłaTanimura, Natsuko, i Kensuke Miyake. "Toll-Like Receptors". W Glycoscience: Biology and Medicine, 1–6. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54836-2_142-1.
Pełny tekst źródłaTanimura, Natsuko, i Kensuke Miyake. "Toll Like Receptors". W Glycoscience: Biology and Medicine, 707–12. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54841-6_142.
Pełny tekst źródłaAllen, Jessica L., Aurelien Trompette i Christopher L. Karp. "Toll-Like Receptors". W Inflammation and Allergy Drug Design, 307–16. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch25.
Pełny tekst źródłaHoebe, Kasper. "Toll-Like Receptors". W Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_5855-2.
Pełny tekst źródłaSzabo, Gyongyi, i Pranoti Mandrekar. "Toll-Like Receptors". W Signaling Pathways in Liver Diseases, 149–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00150-5_9.
Pełny tekst źródłaBrint, Elizabeth, i Philana Fernandes. "Toll-Like Receptors". W Compendium of Inflammatory Diseases, 1266–73. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_176.
Pełny tekst źródłaGazzinelli, Ricardo T., Kate Fitzgerald i Douglas T. Golenbock. "Toll-Like Receptors". W Phagocyte-Pathogen Interactions, 107–22. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816650.ch6.
Pełny tekst źródłaHoebe, Kasper. "Toll-Like Receptors". W Encyclopedia of Cancer, 4580–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_5855.
Pełny tekst źródłaStreszczenia konferencji na temat "Toll-like receptors"
Lim, Kian-Huat, Gregory M. Barton i Louis M. Staudt. "Abstract 2332: OncogenicMYD88mutants require Toll-like receptors." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2332.
Pełny tekst źródłaZayed, Rania. "Toll-like receptors as a potential immunotherapeutic target". W The 9th International conference on Research in Engineering, Science and Technology. Acavent, 2019. http://dx.doi.org/10.33422/9th-rest.2019.04.248.
Pełny tekst źródłaKorbelik, Mladen. "Role of Toll-like receptors in photodynamic-therapy-elicited host response". W Biomedical Optics 2004, redaktorzy Steven L. Jacques i William P. Roach. SPIE, 2004. http://dx.doi.org/10.1117/12.529783.
Pełny tekst źródła"Structure of Toll-like receptors: the input from solution NMR spectroscopy". W Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-171.
Pełny tekst źródłaLebedeva, Olga. "TOLL-LIKE RECEPTORS AND SEVERITY OF ADHESIONS AT WOMEN WITH TUBAL INFERTILITY". W 2nd International Multidisciplinary Scientific Conference on Social Sciences and Arts SGEM2015. Stef92 Technology, 2015. http://dx.doi.org/10.5593/sgemsocial2015/b11/s2.143.
Pełny tekst źródłaJoseph, S., S. Qureshi i BJ Petrof. "Potential Role of Toll-Like Receptors in the Dystrophic (mdx)Mouse Diaphragm." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4191.
Pełny tekst źródłaSartakova, Angelina, Sergei Lukyanov, Andrew Malyarchikov, Jana Shchukina, Alexandra Levanchuk, Arthur Emelyanov i Konstantin Shapovalov. "TOLL-like receptors polymorphism in pneumonia associated with influenza A(H1N1)/09". W ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2325.
Pełny tekst źródłaFang, L., J. Li, L. Zhou, N. Segueni, B. Ryffel, M. Tamm i M. Roth. "Extracellular HSP60 induces airway wall remodeling via Toll-Like-Receptors in mice". W ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.817.
Pełny tekst źródłaSagar, Seil, Kim A. T. Verheijden, Aletta D. Kraneveld, Niki Georgiou, Johan Garssen i Gert Folkerts. "Different Toll-like Receptors (TLRs) And Nod-Like Receptors (NLRs) Expression Profiles In Lung Tissue During Mild And Severe Experimental Asthma". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4183.
Pełny tekst źródłaKnuefermann, P., R. Lohner, O. Boehm, M. Schwederski, R. Meyer i G. Baumgarten. "Cardiac Inflammation and Function during Polymicrobial Sepsis: Differential Role of Toll-Like Receptors." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1146.
Pełny tekst źródłaRaporty organizacyjne na temat "Toll-like receptors"
Beutler, Bruce. Direct Detection of Microbial Infection Through Activation Coupling of the Toll-Like Receptors. Fort Belvoir, VA: Defense Technical Information Center, marzec 2004. http://dx.doi.org/10.21236/ada424869.
Pełny tekst źródłaGraves, David E. Toll Like Receptor-9 Mediated Invasion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2012. http://dx.doi.org/10.21236/ada567128.
Pełny tekst źródłaSelander, Katri. Toll Like Receptor-9 Mediated Invasion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2012. http://dx.doi.org/10.21236/ada567243.
Pełny tekst źródłaGraves, David E. Toll-Like Receptor-9-Mediated Invasion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2011. http://dx.doi.org/10.21236/ada549125.
Pełny tekst źródłaWatkins, Linda R., Steven Maier, Ryan Bachtell, Jonathan Katz i Betty Diamond. Combating Drug Abuse by Targeting Toll-Like Receptor 4 (TLR4). Fort Belvoir, VA: Defense Technical Information Center, październik 2013. http://dx.doi.org/10.21236/ada593126.
Pełny tekst źródłaSelander, Katri. Toll-Like Receptor Pathway as Mediator of Bisphosphonate Effects in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2005. http://dx.doi.org/10.21236/ada439205.
Pełny tekst źródłaNelson, Corwin, Donald C. Beitz, Tim Reinhardt i John Lippolis. Toll-Like Receptor Signaling in Bovine Macrophages Increases 1,25-Dihydroxyvitamin D3 Production. Ames (Iowa): Iowa State University, styczeń 2008. http://dx.doi.org/10.31274/ans_air-180814-482.
Pełny tekst źródłaAbasht, Behnam, Michael G. Kaiser, Jan van der Pool i Susan J. Lamont. Toll-Like Receptor Gene Expression in Cecum and Spleen of Chicks Challenged with Salmonella Enterica Serovar Enteritidis. Ames (Iowa): Iowa State University, styczeń 2008. http://dx.doi.org/10.31274/ans_air-180814-145.
Pełny tekst źródłaMa, Xiaocong, Liying Lu, Yan Tang, Weisheng Luo, Jianxiang Li i Meiwen Tang. Association between Toll-like receptor gene polymorphisms and risk of Helicobacter pylori infection: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, marzec 2021. http://dx.doi.org/10.37766/inplasy2021.3.0009.
Pełny tekst źródłaBaszler, Timothy, Igor Savitsky, Christopher Davies, Lauren Staska i Varda Shkap. Identification of bovine Neospora caninum cytotoxic T-lymphocyte epitopes for development of peptide-based vaccine. United States Department of Agriculture, marzec 2006. http://dx.doi.org/10.32747/2006.7695592.bard.
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