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Książki na temat „Toll-like receptors”

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Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 15 czerwca 2024

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1

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.

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2

McCoy, Claire E., red. 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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3

Fallarino, 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.

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4

O’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.

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5

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

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6

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

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7

Kumar, 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.

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8

Bauer, 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.

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9

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

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

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11

Kielian, Tammy, red. Toll-like Receptors: Roles in Infection and Neuropathology. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00549-7.

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12

Toll-like receptors: Roles in infection and neuropathology. Berlin: Springer Verlag, 2009.

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13

Innate DNA and RNA recognition: Methods and protocols. New York: Humana Press, 2014.

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14

Beutler, Bruce, i Hermann Wagner, red. Toll-Like Receptor Family Members and Their Ligands. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-59430-4.

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15

Quinn, Peter J., i Xiaoyuan Wang. Endotoxins: Structure, function and recognition. Dordrecht: Springer Verlag, 2010.

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16

Rossetti, Carlo, i Francesco Peri, red. The Role of Toll-Like Receptor 4 in Infectious and Non Infectious Inflammation. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-56319-6.

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17

Rezaei, Nima, red. Toll-like Receptors. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.80367.

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18

Konat, Gregory W. Signaling by Toll-Like Receptors. Taylor & Francis Group, 2008.

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19

Konat, Gregory W. Signaling by Toll-Like Receptors. Taylor & Francis Group, 2008.

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20

Toll and Toll-Like Receptors: An Immunologic Perspective. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/b139083.

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21

Rich, Tina. Toll and Toll-Like Receptors : : An Immunologic Perspective. Springer, 2010.

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22

Rich, Tina. Toll and Toll-Like Receptors : : An Immunologic Perspective. Springer London, Limited, 2007.

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23

McCoy, Claire. Toll-Like Receptors: Practice and Methods. Springer New York, 2016.

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24

McCoy, Claire E., i Luke A. J. O'Neill. Toll-Like Receptors: Methods and Protocols. Humana Press, 2011.

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25

McCoy, Claire. Toll-Like Receptors: Practice and Methods. Springer New York, 2018.

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26

Kumar, Vijay. Toll-Like Receptors in Health and Disease. Springer International Publishing AG, 2022.

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27

Hartmann, Gunther, i Stefan Bauer. Toll-Like Receptors (TLRs) and Innate Immunity. Springer Berlin / Heidelberg, 2010.

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28

M. Greene, Catherine, red. Toll-Like Receptors in Diseases of the Lung. BENTHAM SCIENCE PUBLISHERS, 2012. http://dx.doi.org/10.2174/97816080536291120101.

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29

Kielian, Tammy. Toll-Like Receptors: Roles in Infection and Neuropathology. Springer Berlin / Heidelberg, 2012.

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30

Toll and Toll-Like Receptors:: An Immunologic Perspective (Molecular Biology Intelligence Unit). Springer, 2005.

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31

(Editor), Bruce Beutler, i Hermann Wagner (Editor), red. Toll-Like Receptor Familiy Members and Their Ligands. Springer, 2002.

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32

Toll-like receptor family members and their ligands. Berlin: Springer, 2002.

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33

Wagner, Hermann, i Bruce Beutler. Toll-Like Receptor Family Members and Their Ligands. Springer London, Limited, 2011.

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34

Wagner, Hermann, i Bruce Beutler. Toll-Like Receptor Family Members and Their Ligands. Springer London, Limited, 2012.

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35

Konat, Gregory W. Signaling by Toll-Like Receptors. Methods in Signal Transduction Series. Taylor & Francis Group, 2008.

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36

Signaling by Toll-Like Receptors (Methods in Signal Transduction Series). CRC, 2008.

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37

Kircheis, Ralf, i Oliver Planz, red. The Role of Toll-Like Receptors (TLR) in Infection and Inflammation. MDPI, 2023. http://dx.doi.org/10.3390/books978-3-0365-7614-5.

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38

Tolllike Receptors Methods And Protocols. Humana Press, 2009.

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39

Nucleic Acid Sensors and Antiviral Immunity. Taylor & Francis Group, 2012.

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40

Filippi, Christophe M., red. Toll-Like Receptor Activation in Immunity vs. Tolerance. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-636-4.

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41

Wiersinga, W. Joost, i Tom van der Poll. The host response to infection in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0303.

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Infection continues to be a leading cause of intensive care unit death. The host response to infection can be seen as a pattern recognition receptor (PRR)-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. A measured and rapid response to microbial invasion is essential to health. The same immunological and coagulation systems that protect against localized infection can act to our disadvantage when these systems are activated systemically during generalized microbial infection. Toll-like receptors (TLR), the inflammasomes and other PRRs initiate the host response after recognition of pathogen-associated-molecular-patterns (PAMPs) or endogenous danger-associated-molecular-patterns (DAMPs). The systemic host response to infection will result in activation of coagulation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Further dissection of the role of host–pathogen interactions, the cytokine response, the coagulation cascade and their multidirectional interactions in sepsis should lead towards the development of new therapeutic approaches in the critically ill who are faced with infection.
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42

Voll, Reinhard E., i Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
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43

Bonham, Kevin Scott. Cellular and Biochemical Events in Toll-like Receptor Signaling. 2014.

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44

Geri, Guillaume, i Jean-Paul Mira. Host–pathogen interactions in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0306.

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Infection by a pathogenic micro-organism triggers a coordinated activation of both innate and adaptive immune responses. The innate immune response quickly triggers an antimicrobial response that will initiate development of a pathogen-specific, long-lasting adaptive immune response. Accurate recognition of microbial-associated molecular patterns by pattern-recognition receptors (PRRs) is the cornerstone of this immediate response. Most studied PRRs are Toll-like receptors (TLRs) and their kinase signalling cascades that activate nuclear transcription factors, and induce gene expression and cytokine production. Deficiencies or genetic variability in these different signalling pathways may lead to recurrent pyogenic infections and severe invasive diseases. After initial contact between the host and pathogen, numerous factors mediate the inflammatory response, as pro-inflammatory cytokines and chemokines. Apart from host genetic variability, pathogen diversity also influences the phenotypic features of various infectious diseases. Genomic analysis may assist in the development of targeted therapies or new therapeutic strategies based on both patient and microorganism genotype.
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45

Rossetti, Carlo, i Francesco Peri. Role of Toll-Like Receptor 4 in Infectious and Non Infectious Inflammation. Springer International Publishing AG, 2021.

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46

Rossetti, Carlo, i Francesco Peri. Role of Toll-Like Receptor 4 in Infectious and Non Infectious Inflammation. Springer International Publishing AG, 2020.

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47

Quinn, Peter J., i Xiaoyuan Wang. Endotoxins: Structure, Function and Recognition. Springer, 2012.

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48

Quinn, Peter J., i Xiaoyuan Wang. Endotoxins: Structure, Function and Recognition. Springer London, Limited, 2010.

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49

Quinn, Peter J., i Xiaoyuan Wang. Endotoxins: Structure, Function and Recognition. Springer, 2010.

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50

Kelley, Russell Phelps. Modulation of gag-specific cellular immune responses to prototype HIV vaccines by toll-like receptor ligands in mice. 2009.

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