Articoli di riviste: "Toll-like receptors"

1

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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2

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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3

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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4

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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5

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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6

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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7

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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Abstract (sommario):

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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10

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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11

Blasius, Amanda L., and Bruce Beutler. "Intracellular Toll-like Receptors." Immunity 32, no. 3 (March 2010): 305–15. http://dx.doi.org/10.1016/j.immuni.2010.03.012.

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12

Brownlie, Robert, and Brenda Allan. "Avian toll-like receptors." Cell and Tissue Research 343, no. 1 (September 1, 2010): 121–30. http://dx.doi.org/10.1007/s00441-010-1026-0.

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13

Kaisho, Tsuneyasu, and Shizuo Akira. "Toll-like receptors as adjuvant receptors." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1589, no. 1 (February 2002): 1–13. http://dx.doi.org/10.1016/s0167-4889(01)00182-3.

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14

Lipinski, Jay H., Nicole R. Falkowski, Gary B. Huffnagle, John R. Erb-Downward, Robert P. Dickson, Beth B. Moore, and David N. O’Dwyer. "Toll-like receptors, environmental caging, and lung dysbiosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 321, no. 2 (August 1, 2021): L404—L415. http://dx.doi.org/10.1152/ajplung.00002.2021.

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Recent studies have implicated lung microbiota in shaping local alveolar immune responses. Toll-like receptors are major sensors of microbiota and determinants of local epithelial homeostasis. The impact of toll-like receptor deficiency on lung microbiota is unknown. To determine whether the absence of toll-like receptors results in altered lung microbiota or dysbiosis, we compared lung microbiota in wild-type and toll-like receptor-deficient experimental mice using 16S ribosomal RNA gene quantification and sequencing. We used a randomized environmental caging strategy to determine the impact of toll-like receptors on lung microbiota. Lung microbiota are detectable in toll-like receptor-deficient experimental mice and exhibit considerable variability. The lung microbiota of toll-like receptor-deficient mice are altered in community composition (PERMANOVA P < 0.001), display reduced diversity ( t test P = 0.0075), and bacterial burden ( t test P = 0.016) compared with wild-type mice with intact toll-like receptors and associated signaling pathways. The lung microbiota of wild-type mice when randomized to cages with toll-like receptor-deficient mice converged with no significant difference in community composition (PERMANOVA P > 0.05) after 3 wk of cohousing. The lung microbiome of toll-like receptor-deficient mice is distinct from wild-type mice and may be less susceptible to the effects of caging as an environmental variable. Our observations support a role for toll-like receptor signaling in the shaping of lung microbiota.

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15

Mallard, Carina. "Innate Immune Regulation by Toll-Like Receptors in the Brain." ISRN Neurology 2012 (October 14, 2012): 1–19. http://dx.doi.org/10.5402/2012/701950.

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The innate immune system plays an important role in cerebral health and disease. In recent years the role of innate immune regulation by toll-like receptors in the brain has been highlighted. In this paper the expression of toll-like receptors and endogenous toll-like receptor ligands in the brain and their role in cerebral ischemia will be discussed. Further, the ability of systemic toll-like receptor ligands to induce cerebral inflammation will be reviewed. Finally, the capacity of toll-like receptors to both increase (sensitization) and decrease (preconditioning/tolerance) the vulnerability of the brain to damage will be disclosed. Studies investigating the role of toll-like receptors in the developing brain will be emphasized.

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16

Seya, Tsukasa, Masashi Shingai, and Misako Matsumoto. "Toll-like receptors that sense viral infection." Uirusu 54, no. 1 (2004): 1–8. http://dx.doi.org/10.2222/jsv.54.1.

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17

Li, Xia, Dianxuan Guo, Ying Chen та Youdong Hu. "Toll-Like Receptors/TNF-α Pathway Crosstalk and Impact on Different Sites of Recurrent Myocardial Infarction in Elderly Patients". BioMed Research International 2022 (5 квітня 2022): 1–11. http://dx.doi.org/10.1155/2022/1280350.

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Background. Recurrent myocardial infarction is associated with increased mortality. Risk and predictive factors of recurrent myocardial infarction in elderly patients after coronary stenting are not well known. This research sought to investigate the effects of proinflammatory cytokines and toll-like receptor on recurrent myocardial infarction after coronary stenting in elderly patients. Methods. We measured the levels of toll-like receptor 2 (TLR2), toll-like receptor 3 (TLR3), toll-like receptor 4 (TLR4), tumor necrosis factor-α (TNF-α), soluble tumor necrosis factor-α receptor-1 (sTNFR-1), soluble tumor necrosis factor-α receptor-2 (sTNFR-2), endothelial progenitor cells (EPCs), and vascular endothelial growth factor (VEGF) in elderly patients with recurrent myocardial infarction and assessed the changes of proinflammatory cytokines and toll-like receptors in elderly patients with recurrent myocardial infarction after coronary stenting. Results. Levels of TLR2, TLR3, TLR4, TNF-α, sTNFR-1, and sTNFR-2 were remarkably increased ( P < 0.001 ), and EPCs and VEGF were remarkably lowered ( P < 0.001 ) in the elderly patients with recurrent myocardial infarction after coronary stent implantation. Increased expressions of proinflammatory cytokines and toll-like receptors induced recurrent myocardial infarction after coronary stenting. Elevated expressions of proinflammatory cytokines and toll-like receptors may be used to identify elderly patients who have an increased risk of developing recurrent myocardial infarction after coronary stenting. Conclusion. The increase levels of proinflammatory cytokines and toll-like receptors were associated with recurrent myocardial infarction after coronary stenting. Increased expressions of proinflammatory cytokines and toll-like receptors may be clinically useful biomarkers for predicting recurrent myocardial infarction in the elderly patients after coronary stent implantation.

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18

Aksu, Tekin, Neslihan Karakurt, İrem Akar, Yasin Köksal, Fatih M. Azık, Meltem Özgüner, and Duygu Uçkan Çetinkaya. "Toll-Like Receptor Expression of Mesenchymal Stem Cells Derived from Granulocyte Colony-Stimulating Factor Treated Bone Marrow Donors." Acta Medica 51, no. 4 (December 31, 2020): 33–40. http://dx.doi.org/10.32552/2020.actamedica.524.

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Objective: The present study was planned to examine the expression of Toll-like receptors on human marrow-derived mesenchymal stem cells as a result of in-vivo exposure to granulocyte colony-stimulating factor with or without exposure of the cells to Toll-like receptors agonists. Materials and Methods: Toll-like receptor 2, 3, and 4 expressions of mesenchymal stem cells obtained from healthy human bone marrow donors exposed to in-vivo granulocyte colony-stimulating factor were analyzed, and granulocyte colony-stimulating factor untreated donors served as controls. Also, mesenchymal stem cells were stimulated in-vitro by Toll-like receptor agonists to observe the changes in the expression of the Toll-like receptors. Results: Mesenchymal stem cells obtained from both granulocyte colony-stimulating factor exposed or unexposed donors showed a low level of Toll-like receptor 2, 4 expressions by flow cytometry, whereas Toll-like receptor 3 expression was higher. Lipopolysaccharide was used as an agonist, but no significant difference was observed in the Toll-like receptor 2, 4 expressions, both in the granulocyte colony-stimulating factor exposed and unexposed groups. Stimulation of cells with Toll-like receptor 3 ligand was associated with a statistically significant decrease in Toll-like receptor 3 expressions, which was more profound in granulocyte colony-stimulating factor unexposed cells. Conclusion: We have shown that human bone marrow-derived culture-expanded mesenchymal stem cells express Toll-like receptor 3, whether in-vivo granulocyte colony-stimulating factor treated or untreated. Besides, the Toll-like receptor 3 agonist’s effect in lowering the expression levels was more significant in cells that were not exposed to granulocyte colony-stimulating factor. Additionally, detection of low expression of the pro-inflammatory Toll-like receptor 4 versus higher levels of Toll-like receptor 3 supports literature regarding the immunosuppressive characteristics of marrow-derived mesenchymal stem cells. Modulation of the expression of the Toll-like receptor of mesenchymal stem cells with granulocyte colony-stimulating factor or agonists may have implications in allogeneic mesenchymal stem cell therapies.

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19

Mavrouli, M., V. Kapsimali, and A. Tsakris. "The role of Toll-like receptors in innate immunity." ACTA MICROBIOLOGICA HELLENICA 59, no. 4 (December 30, 2014): 7–30. https://doi.org/10.5281/zenodo.10017323.

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Abstract (sommario):

The innate immune system constitutes the first line of defence against invading microbes, which is based on the pattern recognition receptors (PRRs) that recognize molecular patterns associated with pathogens (PAMPs). Toll-like receptors (TLRs), the most distinguished of PRRs, detect potential pathogens and activate intracellular signaling pathways that culminate in the production of proinflammatory mediators. In order to escape from the host inflammatory response, microbes have evolved multiple evasion and subversion strategies. Besides exogenous PAMPs, TLRs can bind with molecular patterns produced by tissue damage or cell apoptosis (DAMPs). Under certain circumstances, this interaction drives to aberrant activation and unrestricted inflammatory responses, contributing to the development of autoimmune diseases. Rare inherited defects of TLR and NF-κB dependent responses and single nucleotide polymorphisms (SNPs) within TLR genes act upon the capacity of the host to mount a proper immune response and are characterized by an increased or altered susceptibility to infectious, inflammatory and allergic diseases. Novel immunotherapeutic approaches are developed based on both activation and inhibition of TLR triggering, and TLR agonists and antagonists have a strong potential for prevention and intervention in infectious diseases. The challenge is to find a balance between the suppression of disease and the retention of the beneficial host immune response.

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20

Falck-Hansen, Mika, Christina Kassiteridi, and Claudia Monaco. "Toll-Like Receptors in Atherosclerosis." International Journal of Molecular Sciences 14, no. 7 (July 4, 2013): 14008–23. http://dx.doi.org/10.3390/ijms140714008.

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21

O'mahony, C., and N. Steedman. "Toll-like receptors: that's weird!" International Journal of STD & AIDS 21, no. 6 (June 2010): 450. http://dx.doi.org/10.1258/ijsa.2010.010184.

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22

Tobias, P. S., and L. K. Curtiss. "Toll-like receptors in atherosclerosis." Biochemical Society Transactions 35, no. 6 (November 23, 2007): 1453–55. http://dx.doi.org/10.1042/bst0351453.

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At one time, atherosclerosis was thought to be a simple lipid storage disease. However, it is now recognized as a chronic and progressive inflammation of the arterial wall. Gene deletion experiments in murine models of atherosclerosis that reduce the inflammatory process also reduce disease severity. Identifying the initiators and mediators of that inflammation can provide promising avenues for prevention or therapy. Two prominent risk factors, hyperlipidaemia and infectious disease, point to innate immune mechanisms as potential contributors to proatherogenic inflammation. The TLRs (Toll-like receptors), pro-inflammatory sensors of pathogens, are potential links between inflammation, infectious disease and atherosclerosis. A mechanism for hyperlipidaemic initiation of sterile inflammation can be postulated because oxidized lipoproteins or their component oxidized lipids have been identified as TLR ligands. Moreover, infectious agents are correlated with atherosclerosis risk. We have identified a role for TLR2 in atherosclerosis in mice deficient in low-density lipoprotein receptor. We observed that proatherogenic TLR2 responses to unknown endogenous or unknown endemic exogenous agonists are mediated by non-BMDC (bone-marrow-derived cells), which can include endothelial cells. In contrast, the proatherogenic TLR2 responses to the defined synthetic exogenous agonist Pam3 CSK4 are mediated at least in part by BMDC, which can include lymphocytes, monocytes/macrophages and dendritic cells. TLR2-mediated cell activation in response to endogenous and exogenous agents is proatherogenic in hyperlipidaemic mice.

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23

Koga, Kaori, and Gil Mor. "Toll-like Receptors and Pregnancy." Reproductive Sciences 14, no. 4 (May 2007): 297–99. http://dx.doi.org/10.1177/1933719107304562.

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24

Espevik, T. "TRAFFICKING OF TOLL-LIKE RECEPTORS." Shock 21, Supplement (March 2004): 10. http://dx.doi.org/10.1097/00024382-200403001-00038.

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25

Fischer, Maria, and Marc Ehlers. "Toll-like Receptors in Autoimmunity." Annals of the New York Academy of Sciences 1143, no. 1 (November 2008): 21–34. http://dx.doi.org/10.1196/annals.1443.012.

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26

Wong, F. Susan, and Li Wen. "Toll-Like Receptors and Diabetes." Annals of the New York Academy of Sciences 1150, no. 1 (December 2008): 123–32. http://dx.doi.org/10.1196/annals.1447.063.

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27

Ermertcan, A. T., F. Öztürk, and K. Gündüz. "Toll-like receptors and skin." Journal of the European Academy of Dermatology and Venereology 25, no. 9 (March 24, 2011): 997–1006. http://dx.doi.org/10.1111/j.1468-3083.2011.04049.x.

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28

Delgado, Mónica A., Rasha A. Elmaoued, Alexander S. Davis, George Kyei, and Vojo Deretic. "Toll-like receptors control autophagy." EMBO Journal 27, no. 7 (March 13, 2008): 1110–21. http://dx.doi.org/10.1038/emboj.2008.31.

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29

Tuon, Felipe F., Valdir S. Amato, Hélio A. Bacha, Tariq AlMusawi, Maria I. Duarte, and Vicente Amato Neto. "Toll-Like Receptors and Leishmaniasis." Infection and Immunity 76, no. 3 (December 10, 2007): 866–72. http://dx.doi.org/10.1128/iai.01090-07.

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30

Miller, Lloyd S. "Toll-Like Receptors in Skin." Advances in Dermatology 24 (November 2008): 71–87. http://dx.doi.org/10.1016/j.yadr.2008.09.004.

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31

Rassa, John C., and Susan R. Ross. "Viruses and Toll-like receptors." Microbes and Infection 5, no. 11 (September 2003): 961–68. http://dx.doi.org/10.1016/s1286-4579(03)00193-x.

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32

Finberg, Robert W., and Evelyn A. Kurt-Jones. "Viruses and Toll-like receptors." Microbes and Infection 6, no. 15 (December 2004): 1356–60. http://dx.doi.org/10.1016/j.micinf.2004.08.013.

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33

Michie, Colin A. "Triage by Toll-like receptors." Trends in Molecular Medicine 8, no. 1 (January 2002): 6. http://dx.doi.org/10.1016/s1471-4914(01)02231-6.

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34

Okun, Eitan, Kathleen J. Griffioen, Justin D. Lathia, Sung-Chun Tang, Mark P. Mattson, and Thiruma V. Arumugam. "Toll-like receptors in neurodegeneration." Brain Research Reviews 59, no. 2 (March 2009): 278–92. http://dx.doi.org/10.1016/j.brainresrev.2008.09.001.

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35

Iribarren, Pablo, and Ji Ming Wang. "Toll-like receptors and diseases." International Immunopharmacology 11, no. 10 (October 2011): 1389–90. http://dx.doi.org/10.1016/j.intimp.2011.08.010.

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36

Ishii, Ken J., and Shizuo Akira. "Toll-like receptors and sepsis." Current Infectious Disease Reports 6, no. 5 (September 2004): 361–66. http://dx.doi.org/10.1007/s11908-004-0034-1.

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37

Kim, G. K., and J. Q. Del Rosso. "Toll-like receptors and skin." Yearbook of Dermatology and Dermatologic Surgery 2012 (January 2012): 334–35. http://dx.doi.org/10.1016/j.yder.2012.02.163.

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38

Rakoff-Nahoum, Seth, and Ruslan Medzhitov. "Toll-like receptors and cancer." Nature Reviews Cancer 9, no. 1 (December 4, 2008): 57–63. http://dx.doi.org/10.1038/nrc2541.

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39

Singh, Madhu V., and François M. Abboud. "Toll-like receptors and hypertension." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 5 (September 1, 2014): R501—R504. http://dx.doi.org/10.1152/ajpregu.00194.2014.

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Abstract (sommario):

Hypertension and associated inflammatory processes that accelerate cardiovascular damage are regulated by the innate immune system. Toll-like receptors (TLR) are major components of the innate immune system that recognize endogenous damage-associated molecular patterns to activate prominent inflammatory signaling including activation of nuclear factor-κB (NF-κB). However, the role of TLR in the etiology of hypertension is not well understood. TLR signaling is dependent on adaptor proteins that, along with the TLR expression patterns, confer specificity of the inflammatory response and its pathological targets. Here we review the conceptual framework of how TLR and their adaptor proteins may differentially affect hypertension and cardiac hypertrophy by different stimuli.

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40

Petry, Vanessa, and Anthony A. Gaspari. "Toll-like receptors and dermatology." International Journal of Dermatology 48, no. 6 (June 2009): 558–70. http://dx.doi.org/10.1111/j.1365-4632.2009.04111.x.

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41

Hurst, Julia, and Philipp von Landenberg. "Toll-like receptors and autoimmunity." Autoimmunity Reviews 7, no. 3 (January 2008): 204–8. http://dx.doi.org/10.1016/j.autrev.2007.11.006.

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42

O'Neill, L. A. J. "Toll-like receptors in cancer." Oncogene 27, no. 2 (January 2008): 158–60. http://dx.doi.org/10.1038/sj.onc.1210903.

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43

Hansbro, Philip M., Tatt Jhong Haw, Malcolm R. Starkey, and Kensuke Miyake. "Toll-like receptors in COPD." European Respiratory Journal 49, no. 5 (May 2017): 1700739. http://dx.doi.org/10.1183/13993003.00739-2017.

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44

Bell, Jennifer. "Living without Toll-like receptors." Nature Reviews Immunology 3, no. 4 (April 2003): 261. http://dx.doi.org/10.1038/nri1073.

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45

Grote, Karsten, Harald Schütt, and Bernhard Schieffer. "Toll-Like Receptors in Angiogenesis." Scientific World JOURNAL 11 (2011): 981–91. http://dx.doi.org/10.1100/tsw.2011.92.

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Abstract (sommario):

Toll-like receptors (TLRs) are known as pattern-recognition receptors related to the Toll protein ofDrosophila. After recognition of pathogen-associated molecular patterns of microbial origin, the TLRs alert the immune system, and initiate innate and adaptive immune responses. The TLR system, though, is not confined solely to the leukocyte-mediated immune defense against exogenous pathogens. Besides myeloid cells, TLR expression has been reported in multiple tissues and cell types, including epithelial and endothelial cells. Moreover, despite the microbial patterns that are commonly accepted as TLR ligands, there is increasing evidence that TLRs also recognize host-derived molecules. In this regard, recent studies point to an involvement of TLRs in various chronic inflammatory disorders and cardiovascular diseases, including atherosclerosis, rheumatoid arthritis, systemic lupus erythematosus, and even cancer. A common feature of these disorders is an enhanced so-called inflammation-induced angiogenesis. However, inflammation-induced angiogenesis is not solely a key component of pathogen defense during acute infection or chronic inflammatory disorders, but also plays a critical role in repair mechanisms, e.g., wound healing and subsequent tissue regeneration. Interestingly, the latest research could coincidentally demonstrate that TLR activation promotes angiogenesis in various inflammatory settings in response to both exogenous and endogenous ligands, although the precise mode of action of TLRs in this context still remains ambiguous. The objective of this review is to present evidence for the implication of TLRs in angiogenesis during physiological and pathophysiological processes, and the potential clinical relevance for new treatment regimes involving TLR modulation.

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46

Fiset, Pierre Olivier, Meri Katarina Tulic, and Qutayba Hamid. "Toll-like receptors and atopy." Journal of Allergy and Clinical Immunology 116, no. 2 (August 2005): 467–70. http://dx.doi.org/10.1016/j.jaci.2005.04.034.

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47

Finberg, Robert W., Jennifer P. Wang, and Evelyn A. Kurt-Jones. "Toll like receptors and viruses." Reviews in Medical Virology 17, no. 1 (2006): 35–43. http://dx.doi.org/10.1002/rmv.525.

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48

Goodsell, David S. "Recognition highlights: Toll-like receptors." Journal of Molecular Recognition 19, no. 5 (2006): 387–88. http://dx.doi.org/10.1002/jmr.778.

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49

Bernard, Marina, and Rosario Rizzuto. "Toll‐like receptors hit calcium." EMBO reports 15, no. 5 (April 2014): 468–69. http://dx.doi.org/10.1002/embr.201438685.

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50

Mempel, Martin, Behnam Naderi Kalali, Markus Ollert, and Johannes Ring. "Toll-Like Receptors in Dermatology." Dermatologic Clinics 25, no. 4 (October 2007): 531–40. http://dx.doi.org/10.1016/j.det.2007.06.014.

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Articoli di riviste sul tema "Toll-like receptors"

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