Relevant bibliographies by topics / Toll-like receptors

Academic literature on the topic 'Toll-like receptors'

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Published: 4 June 2021
Last updated: 15 June 2024

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Journal articles on the topic "Toll-like receptors"

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Lien, Egil, and Robin R. Ingalls. "Toll-like receptors." Critical Care Medicine 30, Suppl. (January 2002): S1—S11. http://dx.doi.org/10.1097/00003246-200201001-00001.

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Erickson, Benjamin, Kirk Sperber, and William H. Frishman. "Toll-Like Receptors." Cardiology in Review 16, no. 6 (November 2008): 273–79. http://dx.doi.org/10.1097/crd.0b013e3181709fd8.

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Warren, H. Shaw. "Toll-like receptors." Critical Care Medicine 33, Suppl (December 2005): S457—S459. http://dx.doi.org/10.1097/01.ccm.0000185504.39347.5d.

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Shin, Ho. "Toll-like Receptors." British Journal of Medicine and Medical Research 3, no. 1 (January 10, 2013): 58–68. http://dx.doi.org/10.9734/bjmmr/2013/2071.

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Muzio, Marta, and Alberto Mantovani. "Toll-like receptors." Microbes and Infection 2, no. 3 (March 2000): 251–55. http://dx.doi.org/10.1016/s1286-4579(00)00303-8.

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Moresco, Eva Marie Y., Diantha LaVine, and Bruce Beutler. "Toll-like receptors." Current Biology 21, no. 13 (July 2011): R488—R493. http://dx.doi.org/10.1016/j.cub.2011.05.039.

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Bilak, H., S. Tauszig-Delamasure, and J. L. Imler. "Toll and Toll-like receptors in Drosophila." Biochemical Society Transactions 31, no. 3 (June 1, 2003): 648–51. http://dx.doi.org/10.1042/bst0310648.

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The Drosophila Toll receptor controls the immune response to Gram-positive bacteria and fungi by activating a signalling pathway partially conserved throughout evolution. The Drosophila genome encodes eight additional Toll-related receptors, most of which appear to carry out developmental rather than immune functions. One exception may be Toll-9, which shares structural and functional similarities with mammalian TLRs.
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Akira, Shizuo. "Mammalian Toll-like receptors." Current Opinion in Immunology 15, no. 1 (February 2003): 5–11. http://dx.doi.org/10.1016/s0952-7915(02)00013-4.

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Akira, Shizuo. "Mammalian Toll-like receptors." Current Opinion in Immunology 15, no. 2 (April 2003): 238. http://dx.doi.org/10.1016/s0952-7915(03)00005-0.

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Modlin, Robert L. "Mammalian Toll-like receptors." Annals of Allergy, Asthma & Immunology 88, no. 6 (June 2002): 543–48. http://dx.doi.org/10.1016/s1081-1206(10)61883-2.

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Dissertations / Theses on the topic "Toll-like receptors"

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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.

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Made available in DSpace on 2014-06-11T19:25:37Z (GMT). No. of bitstreams: 0 Previous issue date: 2009-07-28Bitstream added on 2014-06-13T18:53:48Z : No. of bitstreams: 1 carrenho_lca_me_araca.pdf: 1197310 bytes, checksum: 3d5470911a8b6fe2c7996a8ec61a673a (MD5)
A 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.
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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.

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Irvine, 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.

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Dessing, 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.

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Philbin, 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.

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Cant, 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.

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Naltrexone is an opioid antagonist usually used in the treatment of patients addicted to drugs or alcohol. However, since the 1980s naltrexone has been used at lower doses to treat patients with cancer and autoimmune diseases such as multiple sclerosis and Crohn’s disease. The mechanism of action of naltrexone in treating these diseases is unknown, however, evidence suggests that the drug has immune modulating effects. Toll like receptors (TLR) are type I membrane receptors that are crucial in the innate immune response. TLR recognise exogenous and endogenous ligands to induce the production of proinflammatory cytokines, chemokines and activation markers. Recent studies have suggested that naltrexone antagonises TLR4 and TLR9; providing an insight into the immunomodulatory ability of naltrexone. This thesis examines the effect naltrexone has on TLR expressed within the peripheral blood mononuclear cell (PBMC) population with primary focus on TLR 4 and TLR9. In this study, it was observed that naltrexone inhibits IL-6 produced by immune cell subsets following stimulation of TLR2, TLR7 and TLR9, but contrary to previous studies no inhibition of TLR4 was observed. Furthermore, it was determined that apoptosis is not induced under any condition. Studies examining isolated immune cell subsets demonstrated that naltrexone can modulate IL-6 production following stimulation of TLR7/8 on monocytes and TLR9 on B cells. However, naltrexone had no effect on B cell differentiation following stimulation with TLR9 ligand. This study is the first to examine the effect naltrexone has on human immune cells and the findings presented suggest naltrexone has the potential to modulate the production of cytokine in response to TLR activation. Therefore, this study provides preliminary evidence to support the hypothesis that naltrexone modulates TLR activity however, further research is required to justify the use of the drug as an immune modulator in patients with autoimmune diseases and cancer.
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Kassem, 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.

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Patients with inflammatory or infectious conditions such as periodontitis, peri-implantitis, osteomyelitis, rheumatoid arthritis, septic arthritis and loosened joint prosthesis display varying severity of destruction in the adjacent bone tissue. Bone loss in inflammatory diseases is considered a consequence of cytokine induced RANKL and subsequent enhanced osteoclast formation. Hence, osteotropic cytokines and their receptors have been suggested to be important for the pathogenesis of inflammation-induced osteolysis. It is, here, suggested that bacterial components, so called “pathogen associated molecular patterns=PAMPs”, may also be involved. Varieties of cells express receptors for PAMPs, including Toll-like receptors (TLRs) which are the first line of defence in the innate immune system. LPS (lipopolysaccharide), fimbria and lipoproteins from pathogenic bacteria such as P. gingivalis, S. aureus are ligands for TLR2 and flagellin from pathogenic flagellated bacteria like S. typhimurium is a ligand for TLR5.   Since the susceptibility to, or the severity of inflammation-associated bone diseases are likely related to differences in the tissue response, and the mechanisms by which PAMPs interact with bone cells are not fully understood, we aimed to elucidate the importance of different TLRs for inflammation induced bone loss by conducting in vitro and in vivo investigations. Activation of TLR2 and TLR5 in organ cultured mouse parietal bones increased bone resorption in a time- and concentration-dependent manner by a process inhibited by OPG and bisphosphonate, showing the crucial role of RANKL-induced osteoclast formation. In addition, the number of osteoclasts, expression of osteoclastic genes and osteoclastogenic transcription factors were increased. In the bones and in osteoblasts isolated from the bones, TLR2 agonists increased the expression of RANKL without affecting OPG, while TLR5 activation resulted in enhanced RANKL and decreased OPG. Activation of both TLR2 and TLR5 stimulated the expression in both bones and osteoblasts of prostaglandins and pro-inflammatory cytokines, known to stimulate RANKL. By blocking the cytokines and prostaglandin, we showed that TLR2 and TLR5 induced bone resorption and RANKL expression are independent of these molecules. Activation of TLR2, but not TLR5, in mouse bone marrow macrophage cultures inhibited RANKL-induced osteoclast formation, an effect not observed in committed pre-osteoclasts. Local administration in vivo of TLR2 and TLR5 agonists on the top of mouse skull bones enhanced local and systemic osteoclast formation and bone resorption. Using knockout mice, we showed that the effects by LPS from P. gingivalis (used as TLR2 agonist) and flagellins (used as TLR5 agonists) are explicit for TLR2 and TLR5 ex vivo and in vivo, respectively. These data show that stimulation of TLR2 and TLR5 results in bone resorption in vitro and in vivo mediated by increased RANKL in osteoblasts and thus may be one mechanism for developing inflammatory bone loss. Interestingly, histological analyses of skull bones of mice treated locally with TLR2 and TLR5 agonists revealed that the bones not only reacted with locally increased osteoclastogenesis (osteoclast formation), but also with locally increased new bone formation. This was observed on both periosteal and endosteal sides of the bones, as well as in the bone marrow compartment. The formation of new bone was seen close to osteoclasts in some parts, but also in other areas, distant from these cells. The response was associated with active, cuboidal osteoblasts, extensive cell proliferation and increased expression of genes coding for bone matrix proteins and osteoblastic transcription factors. In conclusion, activation of TLR2 and TLR5 in osteoblasts results in bone loss associated with enhanced osteoclast formation and bone resorption, as well as with increased osteoblast differentiation and new bone formation, indicating that inflammation causes bone modeling. The data provide an explanation why LPS from P. gingivalis and flagellin from flagella-expressing bacteria can stimulate bone loss. Since TLR2 and TLR5 can be activated not only by bacterial components, but also by endogenous ligands produced in inflammatory processes, the data also contribute to the understanding of inflammation induced bone loss in autoimmune diseases. Hopefully, these findings will contribute to the development of treatment strategies for inflammation induced bone loss.
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Weber, 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.

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Braedel-Ruoff, Sibylla. "Toll-like receptors - link between innate and adaptive immunity." [S.l. : s.n.], 2007.

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Estévez, Medina Javier. "Toll-like receptors as modulators of intestinal barrier function." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/400146.

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Las patologías funcionales (síndrome del intestino irritable, IBS) e inflamatorias gastrointestinales (enfermedad inflamatoria intestinal, IBD) se caracterizan por alteraciones de la función barrera epitelial, con un aumento de la permeabilidad, y cambios en la microbiota intestinal. Los receptores de tipo Toll (TLRs) participan en el reconocimiento bacteriano en el intestino y en el control neuroinmune local, estando, por tanto, implicados en la regulación de la función barrera del epitelio intestinal. El objetivo de este trabajo ha sido caracterizar la implicación de los receptores TLR5 y TLR7 en la regulación de la función barrera epitelial del colon. Para ello se ha caracterizado la función barrera epitelial, tanto en condiciones in vitro (electrofisiología y permeabilidad a macromoléculas en un sistema de cámaras de Ussing), como in vivo (permeabilidad a macromoléculas), tras la sobre-estimulación local de los receptores TLR5 y TLR7 con agonistas selectivos, flagelina e imiquimod, respectivamente, en rata y ratón. Los efectos en la función barrera se han caracterizado en condiciones normales, en estados de permeabilización del epitelio con DMSO, y en condiciones de inflamación (colitis inducida por dextrano sulfato de sodio -DSS-). Con la finalidad de definir el mecanismo de acción, se ha valorado la dinámica de las uniones estrechas epiteliales (expresión génica de proteínas -RT-qPCR- y distribución celular -inmunohistoquímica-) y la activación inmune local (expresión de citoquinas pro-inflamatorias). Los resultados obtenidos muestran que la sobre-estimulación del TLR7 del colon in vivo mejora la función barrera epitelial en la rata en condiciones fisiológicas, observando una reducción dosis-dependiente de la permeabilidad epitelial a macromoléculas evaluada en las cámaras de Ussing. No obstante, en condiciones de permeabilización del epitelio con DMSO, la sobre-estimulación del TLR7 causa un empeoramiento de la función barrera valorada in vivo. En ratones, la sobre-estimulación del TLR7 cólico in vitro no tiene efecto. Sin embargo, en un modelo de colitis inducida por DSS, reduce el aumento de la permeabilidad epitelial causado por la inflamación. Por tanto, parecen existir diferencias especie-específicas en los efectos de la sobre-estimulación del TLR7 cólico, pudiéndose observar tanto acciones promotoras como lesivas de la función barrera epitelial. La sobre-estimulación del TLR5 cólico agrava la disfunción de la barrera asociada a la inflamación (colitis inducida por DSS) en el ratón, incrementando la permeabilidad a macromoléculas. Sin embargo, la adición del agonista del TLR5, flagelina, en las cámaras de Ussing no afecta a la función barrera epitelial, ni en condiciones fisiológicas, ni durante la inflamación. En ningún caso, estos efectos moduladores de la función barrera se asociaron a cambios en la expresión génica de las principales proteínas de las uniones estrechas (claudina-2, claudina-3, ocludina, tricelulina, molécula de adhesión de la unión de tipo 1 y Zonula Occludens 1) ni a su distribución celular (claudina-2, claudina-3 y ZO-1). De la misma forma, los factores moduladores de la barrera, quinasa de la cadena ligera de la miosina y pro-glucagón (precursor del péptido similar al glucagón de tipo 2), tampoco presentaron cambios en su expresión asociados a la sobre-estimulación del TLR5 o del TLR7. Finalmente, se observó un efecto inmunomodulador receptor-específico. La sobre-estimulación del TLR7 reveló efectos potencialmente protectores al reducir la expresión de la citoquina pro-inflamatoria IL12-p40. Por el contrario, la sobre-estimulación del TLR5 tendió a aumentar la expresión de marcadores pro-inflamatorios, sugiriendo, por tanto, efectos pro-lesivos. En conclusión, estos resultados muestran la importancia de las interacciones microbiota-hospedador mediadas por TLRs en el control de la función barrera epitelial intestinal. Tanto el TLR7 como el TLR5 cólicos pueden considerarse potenciales dianas terapéuticas para el control de la función barrera y las respuestas inmunes locales en desórdenes funcionales e inflamatorios gastrointestinales como el IBD y el IBS.
Functional (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.
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Books on the topic "Toll-like receptors"

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McCoy, Claire E., and Luke A. J. O’Neill, eds. Toll-Like Receptors. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-541-1.

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McCoy, Claire E., ed. Toll-Like Receptors. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3335-8.

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Fallarino, Francesca, Marco Gargaro, and Giorgia Manni, eds. Toll-Like Receptors. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3366-3.

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O’Neill, Luke A. J., and Elizabeth Brint, eds. Toll-like Receptors in Inflammation. Basel: Birkhäuser Basel, 2005. http://dx.doi.org/10.1007/3-7643-7441-1.

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J, O'Neill Luke A., and Brint Elizabeth, eds. Toll-like receptors in inflammation. Basel: Birkhäuser Verlag, 2005.

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W, Konat Gregory, ed. Signaling by toll-like receptors. Boca Raton: Taylor & Francis Group, 2008.

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Kumar, Vijay, ed. Toll-like Receptors in Health and Disease. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-06512-5.

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Bauer, Stefan, and Gunther Hartmann, eds. Toll-Like Receptors (TLRs) and Innate Immunity. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-72167-3.

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Prof, Bauer Stefan, Hartmann Gunther 1966-, and Akira S, eds. Toll-like receptors (TLRs) and innate immunity. Berlin: Springer, 2008.

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Prof, Bauer Stefan, Hartmann Gunther 1966-, and Akira S, eds. Toll-like receptors (TLRs) and innate immunity. Berlin: Springer, 2008.

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Book chapters on the topic "Toll-like receptors"

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Shiu, Jessica, and Anthony A. Gaspari. "Toll-Like Receptors." In Clinical and Basic Immunodermatology, 11–34. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-29785-9_2.

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Pugin, Jérôme. "Toll-Like Receptors." In 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.

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Tanimura, Natsuko, and Kensuke Miyake. "Toll-Like Receptors." In Glycoscience: Biology and Medicine, 1–6. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54836-2_142-1.

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Tanimura, Natsuko, and Kensuke Miyake. "Toll Like Receptors." In Glycoscience: Biology and Medicine, 707–12. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54841-6_142.

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Allen, Jessica L., Aurelien Trompette, and Christopher L. Karp. "Toll-Like Receptors." In Inflammation and Allergy Drug Design, 307–16. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch25.

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Hoebe, Kasper. "Toll-Like Receptors." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_5855-2.

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Szabo, Gyongyi, and Pranoti Mandrekar. "Toll-Like Receptors." In 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.

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Brint, Elizabeth, and Philana Fernandes. "Toll-Like Receptors." In Compendium of Inflammatory Diseases, 1266–73. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_176.

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Gazzinelli, Ricardo T., Kate Fitzgerald, and Douglas T. Golenbock. "Toll-Like Receptors." In Phagocyte-Pathogen Interactions, 107–22. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816650.ch6.

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Hoebe, Kasper. "Toll-Like Receptors." In Encyclopedia of Cancer, 4580–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_5855.

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Conference papers on the topic "Toll-like receptors"

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Lim, Kian-Huat, Gregory M. Barton, and Louis M. Staudt. "Abstract 2332: OncogenicMYD88mutants require Toll-like receptors." In 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.

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Zayed, Rania. "Toll-like receptors as a potential immunotherapeutic target." In The 9th International conference on Research in Engineering, Science and Technology. Acavent, 2019. http://dx.doi.org/10.33422/9th-rest.2019.04.248.

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Korbelik, Mladen. "Role of Toll-like receptors in photodynamic-therapy-elicited host response." In Biomedical Optics 2004, edited by Steven L. Jacques and William P. Roach. SPIE, 2004. http://dx.doi.org/10.1117/12.529783.

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"Structure of Toll-like receptors: the input from solution NMR spectroscopy." In 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.

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Lebedeva, Olga. "TOLL-LIKE RECEPTORS AND SEVERITY OF ADHESIONS AT WOMEN WITH TUBAL INFERTILITY." In 2nd International Multidisciplinary Scientific Conference on Social Sciences and Arts SGEM2015. Stef92 Technology, 2015. http://dx.doi.org/10.5593/sgemsocial2015/b11/s2.143.

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Joseph, S., S. Qureshi, and BJ Petrof. "Potential Role of Toll-Like Receptors in the Dystrophic (mdx)Mouse Diaphragm." In 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.

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Sartakova, Angelina, Sergei Lukyanov, Andrew Malyarchikov, Jana Shchukina, Alexandra Levanchuk, Arthur Emelyanov, and Konstantin Shapovalov. "TOLL-like receptors polymorphism in pneumonia associated with influenza A(H1N1)/09." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2325.

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Fang, L., J. Li, L. Zhou, N. Segueni, B. Ryffel, M. Tamm, and M. Roth. "Extracellular HSP60 induces airway wall remodeling via Toll-Like-Receptors in mice." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.817.

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Sagar, Seil, Kim A. T. Verheijden, Aletta D. Kraneveld, Niki Georgiou, Johan Garssen, and Gert Folkerts. "Different Toll-like Receptors (TLRs) And Nod-Like Receptors (NLRs) Expression Profiles In Lung Tissue During Mild And Severe Experimental Asthma." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4183.

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Knuefermann, P., R. Lohner, O. Boehm, M. Schwederski, R. Meyer, and G. Baumgarten. "Cardiac Inflammation and Function during Polymicrobial Sepsis: Differential Role of Toll-Like Receptors." In 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.

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Reports on the topic "Toll-like receptors"

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Beutler, Bruce. Direct Detection of Microbial Infection Through Activation Coupling of the Toll-Like Receptors. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada424869.

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Graves, David E. Toll Like Receptor-9 Mediated Invasion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada567128.

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Selander, Katri. Toll Like Receptor-9 Mediated Invasion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada567243.

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Graves, David E. Toll-Like Receptor-9-Mediated Invasion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada549125.

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Watkins, Linda R., Steven Maier, Ryan Bachtell, Jonathan Katz, and Betty Diamond. Combating Drug Abuse by Targeting Toll-Like Receptor 4 (TLR4). Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada593126.

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Selander, Katri. Toll-Like Receptor Pathway as Mediator of Bisphosphonate Effects in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada439205.

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Nelson, Corwin, Donald C. Beitz, Tim Reinhardt, and John Lippolis. Toll-Like Receptor Signaling in Bovine Macrophages Increases 1,25-Dihydroxyvitamin D3 Production. Ames (Iowa): Iowa State University, January 2008. http://dx.doi.org/10.31274/ans_air-180814-482.

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Abasht, Behnam, Michael G. Kaiser, Jan van der Pool, and 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, January 2008. http://dx.doi.org/10.31274/ans_air-180814-145.

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Ma, Xiaocong, Liying Lu, Yan Tang, Weisheng Luo, Jianxiang Li, and 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, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0009.

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Baszler, Timothy, Igor Savitsky, Christopher Davies, Lauren Staska, and Varda Shkap. Identification of bovine Neospora caninum cytotoxic T-lymphocyte epitopes for development of peptide-based vaccine. United States Department of Agriculture, March 2006. http://dx.doi.org/10.32747/2006.7695592.bard.

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Abstract:
The goal of the one-year feasibility study was to identify specific cytotoxic T-lymphocyte (CTL) epitopes to Neosporacaninum in the natural bovine host in order to make progress toward developing an effective peptide-based vaccine against bovine neosporosis. We tested the hypothesis that: N. caninum SRS2 peptides contain immunogenicCTLepitope clusters cross-presented by multiple bovine MHC-I and MHC-IIhaplotypes. The specific objectives were: (1) Map bovine CTLepitopes of N. caninum NcSRS-2 and identify consensus MHC-I and class-II binding motifs; and (2) Determine if subunit immunization with peptides containing N. caninum-specificCTLepitopes cross-reactive to multiple bovine MHChaplotypes induces a CTL response in cattle with disparate MHChaplotypes. Neosporosis is a major cause of infectious abortion and congenital disease in cattle, persisting in cattle herds via vertical transmission.5 N. caninum abortions are reported in Israel; a serological survey of 52 Israeli dairy herds with reported abortions indicated a 31% infection rate in cows and 16% infection rate in aborted fetuses.9,14 Broad economic loss due to bovine neosporosis is estimated at $35,000,000 per year in California, USA, and $100,000,000 (Australian) per year in Australia and New Zealand.13 Per herd losses in a Canadian herd of 50 cattle are estimated more conservatively at $2,305 (Canadian) annually.4 Up to date practical measures to reduce losses from neosporosis in cattle have not been achieved. There is no chemotherapy available and, although progress has been made toward understanding immunity to Neospora infections, no efficacious vaccine is available to limit outbreaks or prevent abortions. Vaccine development to prevent N. caninum abortion and congenital infection remains a high research priority. To this end, our research group has over the past decade: 1) Identified the importance of T-lymphocyte-mediated immunity, particularly IFN-γ responses, as necessary for immune protection to congenital neosporosis in mice,1,2,10,11 and 2) Identified MHC class II restricted CD4+ CTL in Neosporainfected Holstein cattle,16 and 3) Identified NcSRS2 as a highly conserved surface protein associated with immunity to Neospora infections in mice and cattle.7,8,15 In this BARD-funded 12 month feasibility study, we continued our study of Neospora immunity in cattle and successfully completed T-lymphocyte epitope mapping of NcSRS2 surface protein with peptides and bovine immune cells,15 fulfilling objective 1. We also documented the importance of immune responses NcSRS2 by showing that immunization with native NcSRS2 reduces congenital Neospora transmission in mice,7 and that antibodies to NcSRS2 specifically inhibition invasion of placental trophoblasts.8 Most importantly we showed that T-lymphocyte responses similar to parasite infection, namely induction of activated IFN-γ secreting Tlymphocytes, could be induced by subunit immunization with NcSRS2 peptides containing the Neospora-specificCTLepitopes (Baszler et al, In preparation) fulfilling objective 2. Both DNA and peptide-based subunit approaches were tested. Only lipopeptide-based NcSRS2 subunits, modified with N-terminal linked palmitic acid to enhance Toll-like receptors 2 and 1 (TLR2-TLR1), stimulated robust antigen-specific T-lymphocyte proliferation, IFN-γ secretion, and serum antibody production across different MHC-IIhaplotypes. The discovery of MHC-II cross-reactive T-cellinducing parasite peptides capable of inducing a potentially protective immune response following subunit immunization in cattle is of significant practical importance to vaccine development to bovine neosporosis. In addition, our findings are more widely applicable in future investigations of protective T-cell, subunit-based immunity against other infectious diseases in outbred cattle populations.
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