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Erschienen in: Seminars in Immunopathology 3/2007

01.09.2007 | Review

Inflammasomes in inflammatory disorders: the role of TLRs and their interactions with NLRs

verfasst von: Christine E. Becker, Luke A. J. O’Neill

Erschienen in: Seminars in Immunopathology | Ausgabe 3/2007

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Abstract

The innate immune system relies on a variety of pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs) to sense microbial structures that are present in pathogens. Various levels of crosstalk between the TLR and NLR pathways have been described, most notably the description of a molecular scaffold complex, termed the inflammasome, which requires input from both pathways and leads to the activation of the proinflammatory cytokines interleukin (IL)-1β and IL-18. In certain cases, the inflammatory process becomes dysregulated and chronic inflammatory diseases may develop. Understanding the interactions of the TLR and NLR pathways will provide further clues to the pathogeneses of these diseases and to the development of efficient therapies to combat them.
Literatur
1.
Zurück zum Zitat O’Neill LA (2006) How Toll-like receptors signal: what we know and what we don’t know. Curr Opin Immunol 18(1):3–9PubMedCrossRef O’Neill LA (2006) How Toll-like receptors signal: what we know and what we don’t know. Curr Opin Immunol 18(1):3–9PubMedCrossRef
2.
Zurück zum Zitat Bowie A, O’Neill LA (2000) The interleukin-1 receptor/Toll-like receptor superfamily: signal generators for pro-inflammatory interleukins and microbial products. J Leukoc Biol 67(4):508–514PubMed Bowie A, O’Neill LA (2000) The interleukin-1 receptor/Toll-like receptor superfamily: signal generators for pro-inflammatory interleukins and microbial products. J Leukoc Biol 67(4):508–514PubMed
4.
Zurück zum Zitat Creagh EM, O’Neill LA (2006) TLRs, NLRs and RLRs: a trinity of pathogen sensors that co-operate in innate immunity. Trends Immunol 27(8):352–357PubMedCrossRef Creagh EM, O’Neill LA (2006) TLRs, NLRs and RLRs: a trinity of pathogen sensors that co-operate in innate immunity. Trends Immunol 27(8):352–357PubMedCrossRef
6.
Zurück zum Zitat Kawai T et al (2004) Interferon-alpha induction through Toll-like receptors involves a direct interaction of IRF7 with MyD88 and TRAF6. Nat Immunol 5(10):1061–1068PubMedCrossRef Kawai T et al (2004) Interferon-alpha induction through Toll-like receptors involves a direct interaction of IRF7 with MyD88 and TRAF6. Nat Immunol 5(10):1061–1068PubMedCrossRef
7.
Zurück zum Zitat Honda K et al (2004) Role of a transductional–transcriptional processor complex involving MyD88 and IRF-7 in Toll-like receptor signaling. Proc Natl Acad Sci U S A 101(43):15416–15421PubMedCrossRef Honda K et al (2004) Role of a transductional–transcriptional processor complex involving MyD88 and IRF-7 in Toll-like receptor signaling. Proc Natl Acad Sci U S A 101(43):15416–15421PubMedCrossRef
8.
Zurück zum Zitat Takaoka A et al (2005) Integral role of IRF-5 in the gene induction programme activated by Toll-like receptors. Nature 434(7030):243–249PubMedCrossRef Takaoka A et al (2005) Integral role of IRF-5 in the gene induction programme activated by Toll-like receptors. Nature 434(7030):243–249PubMedCrossRef
9.
Zurück zum Zitat Yamamoto M et al (2003) Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway. Science 301(5633):640–643PubMedCrossRef Yamamoto M et al (2003) Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway. Science 301(5633):640–643PubMedCrossRef
10.
Zurück zum Zitat Oshiumi H et al (2003) TIR-containing adapter molecule (TICAM)-2, a bridging adapter recruiting to toll-like receptor 4 TICAM-1 that induces interferon-beta. J Biol Chem 278(50):49751–49762PubMedCrossRef Oshiumi H et al (2003) TIR-containing adapter molecule (TICAM)-2, a bridging adapter recruiting to toll-like receptor 4 TICAM-1 that induces interferon-beta. J Biol Chem 278(50):49751–49762PubMedCrossRef
11.
Zurück zum Zitat Meylan E et al (2004) RIP1 is an essential mediator of Toll-like receptor 3-induced NF-kappa B activation. Nat Immunol 5(5):503–507PubMedCrossRef Meylan E et al (2004) RIP1 is an essential mediator of Toll-like receptor 3-induced NF-kappa B activation. Nat Immunol 5(5):503–507PubMedCrossRef
12.
Zurück zum Zitat Fitzgerald KA et al (2001) Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction. Nature 413(6851):78–83PubMedCrossRef Fitzgerald KA et al (2001) Mal (MyD88-adapter-like) is required for Toll-like receptor-4 signal transduction. Nature 413(6851):78–83PubMedCrossRef
13.
Zurück zum Zitat Carty M et al (2006) The human adaptor SARM negatively regulates adaptor protein TRIF-dependent Toll-like receptor signaling. Nat Immunol 7(10):1074–1081PubMedCrossRef Carty M et al (2006) The human adaptor SARM negatively regulates adaptor protein TRIF-dependent Toll-like receptor signaling. Nat Immunol 7(10):1074–1081PubMedCrossRef
14.
Zurück zum Zitat Liew FY et al (2005) Negative regulation of toll-like receptor-mediated immune responses. Nat Rev Immunol 5(6):446–458PubMedCrossRef Liew FY et al (2005) Negative regulation of toll-like receptor-mediated immune responses. Nat Rev Immunol 5(6):446–458PubMedCrossRef
15.
Zurück zum Zitat Ting JP, Kastner DL, Hoffman HM (2006) CATERPILLERs, pyrin and hereditary immunological disorders. Nat Rev Immunol 6(3):183–195PubMedCrossRef Ting JP, Kastner DL, Hoffman HM (2006) CATERPILLERs, pyrin and hereditary immunological disorders. Nat Rev Immunol 6(3):183–195PubMedCrossRef
16.
Zurück zum Zitat Werts C, Girardin SE, Philpott DJ (2006) TIR, CARD and PYRIN: three domains for an antimicrobial triad. Cell Death Differ 13(5):798–815PubMedCrossRef Werts C, Girardin SE, Philpott DJ (2006) TIR, CARD and PYRIN: three domains for an antimicrobial triad. Cell Death Differ 13(5):798–815PubMedCrossRef
17.
Zurück zum Zitat Barnich N et al (2005) Membrane recruitment of NOD2 in intestinal epithelial cells is essential for nuclear factor-{kappa}B activation in muramyl dipeptide recognition. J Cell Biol 170(1):21–26PubMedCrossRef Barnich N et al (2005) Membrane recruitment of NOD2 in intestinal epithelial cells is essential for nuclear factor-{kappa}B activation in muramyl dipeptide recognition. J Cell Biol 170(1):21–26PubMedCrossRef
18.
Zurück zum Zitat Kummer JA et al (2007) Inflammasome components NALP 1 and 3 show distinct but separate expression profiles in human tissues, suggesting a site-specific role in the inflammatory response. J Histochem Cytochem 55(5):443–452PubMedCrossRef Kummer JA et al (2007) Inflammasome components NALP 1 and 3 show distinct but separate expression profiles in human tissues, suggesting a site-specific role in the inflammatory response. J Histochem Cytochem 55(5):443–452PubMedCrossRef
19.
Zurück zum Zitat LeibundGut-Landmann S et al (2004) Mini-review: specificity and expression of CIITA, the master regulator of MHC class II genes. Eur J Immunol 34(6):1513–1525PubMedCrossRef LeibundGut-Landmann S et al (2004) Mini-review: specificity and expression of CIITA, the master regulator of MHC class II genes. Eur J Immunol 34(6):1513–1525PubMedCrossRef
20.
Zurück zum Zitat Chamaillard M, Inohara,N, Nunez G (2004) Battling enteroinvasive bacteria: Nod1 comes to the rescue. Trends Microbiol 12(12):529–532PubMedCrossRef Chamaillard M, Inohara,N, Nunez G (2004) Battling enteroinvasive bacteria: Nod1 comes to the rescue. Trends Microbiol 12(12):529–532PubMedCrossRef
21.
Zurück zum Zitat Girardin SE et al (2003) Nod1 detects a unique muropeptide from gram-negative bacterial peptidoglycan. Science 300(5625):1584–1587PubMedCrossRef Girardin SE et al (2003) Nod1 detects a unique muropeptide from gram-negative bacterial peptidoglycan. Science 300(5625):1584–1587PubMedCrossRef
22.
Zurück zum Zitat Inohara N et al (2003) Host recognition of bacterial muramyl dipeptide mediated through NOD2. Implications for Crohn’s disease. J Biol Chem 278(8):5509–5512PubMedCrossRef Inohara N et al (2003) Host recognition of bacterial muramyl dipeptide mediated through NOD2. Implications for Crohn’s disease. J Biol Chem 278(8):5509–5512PubMedCrossRef
23.
Zurück zum Zitat Girardin SE et al (2003) Nod2 is a general sensor of peptidoglycan through muramyl dipeptide (MDP) detection. J Biol Chem 278(11):8869–8872PubMedCrossRef Girardin SE et al (2003) Nod2 is a general sensor of peptidoglycan through muramyl dipeptide (MDP) detection. J Biol Chem 278(11):8869–8872PubMedCrossRef
24.
Zurück zum Zitat Meylan E, Tschopp J (2005) The RIP kinases: crucial integrators of cellular stress. Trends Biochem Sci 30(3):151–159PubMedCrossRef Meylan E, Tschopp J (2005) The RIP kinases: crucial integrators of cellular stress. Trends Biochem Sci 30(3):151–159PubMedCrossRef
25.
Zurück zum Zitat Kobayashi KS et al (2005) Nod2-dependent regulation of innate and adaptive immunity in the intestinal tract. Science 307(5710):731–734PubMedCrossRef Kobayashi KS et al (2005) Nod2-dependent regulation of innate and adaptive immunity in the intestinal tract. Science 307(5710):731–734PubMedCrossRef
26.
Zurück zum Zitat Girardin SE et al (2001) CARD4/Nod1 mediates NF-kappaB and JNK activation by invasive Shigella flexneri. EMBO Rep 2(8):736–742PubMedCrossRef Girardin SE et al (2001) CARD4/Nod1 mediates NF-kappaB and JNK activation by invasive Shigella flexneri. EMBO Rep 2(8):736–742PubMedCrossRef
27.
Zurück zum Zitat Boyden ED, Dietrich WF (2006) Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin. Nat Genet 38(2):240–244PubMedCrossRef Boyden ED, Dietrich WF (2006) Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin. Nat Genet 38(2):240–244PubMedCrossRef
28.
Zurück zum Zitat Agostini L et al (2004) NALP3 forms an IL-1beta-processing inflammasome with increased activity in Muckle–Wells autoinflammatory disorder. Immunity 20(3):319–325PubMedCrossRef Agostini L et al (2004) NALP3 forms an IL-1beta-processing inflammasome with increased activity in Muckle–Wells autoinflammatory disorder. Immunity 20(3):319–325PubMedCrossRef
29.
Zurück zum Zitat Park JH et al (2007) RICK/RIP2 mediates innate immune responses induced through Nod1 and Nod2 but not TLRs. J Immunol 178(4):2380–2386PubMed Park JH et al (2007) RICK/RIP2 mediates innate immune responses induced through Nod1 and Nod2 but not TLRs. J Immunol 178(4):2380–2386PubMed
30.
Zurück zum Zitat Mariathasan S et al (2004) Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf. Nature 430(6996):213–218PubMedCrossRef Mariathasan S et al (2004) Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf. Nature 430(6996):213–218PubMedCrossRef
31.
Zurück zum Zitat Sutterwala FS et al (2006) Critical role for NALP3/CIAS1/cryopyrin in innate and adaptive immunity through its regulation of caspase-1. Immunity 24(3):317–327PubMedCrossRef Sutterwala FS et al (2006) Critical role for NALP3/CIAS1/cryopyrin in innate and adaptive immunity through its regulation of caspase-1. Immunity 24(3):317–327PubMedCrossRef
32.
Zurück zum Zitat Watanabe H et al (2007) Activation of the IL-1beta-processing inflammasome is involved in contact hypersensitivity. J Invest Dermatol (in press) Watanabe H et al (2007) Activation of the IL-1beta-processing inflammasome is involved in contact hypersensitivity. J Invest Dermatol (in press)
33.
Zurück zum Zitat O’Neill LA (2000) The interleukin-1 receptor/Toll-like receptor superfamily: signal transduction during inflammation and host defense. Sci STKE 2000(44):RE1 O’Neill LA (2000) The interleukin-1 receptor/Toll-like receptor superfamily: signal transduction during inflammation and host defense. Sci STKE 2000(44):RE1
34.
Zurück zum Zitat Martinon F, Tschopp J (2005) NLRs join TLRs as innate sensors of pathogens. Trends Immunol 26(8):447–454PubMedCrossRef Martinon F, Tschopp J (2005) NLRs join TLRs as innate sensors of pathogens. Trends Immunol 26(8):447–454PubMedCrossRef
35.
Zurück zum Zitat Takeuchi O et al (1999) Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components. Immunity 11(4):443–451PubMedCrossRef Takeuchi O et al (1999) Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components. Immunity 11(4):443–451PubMedCrossRef
36.
Zurück zum Zitat Travassos LH et al (2004) Toll-like receptor 2-dependent bacterial sensing does not occur via peptidoglycan recognition. EMBO Rep 5(10):1000–1006PubMedCrossRef Travassos LH et al (2004) Toll-like receptor 2-dependent bacterial sensing does not occur via peptidoglycan recognition. EMBO Rep 5(10):1000–1006PubMedCrossRef
37.
Zurück zum Zitat Fritz JH et al (2005) Synergistic stimulation of human monocytes and dendritic cells by Toll-like receptor 4 and NOD1- and NOD2-activating agonists. Eur J Immunol 35(8):2459–2470PubMedCrossRef Fritz JH et al (2005) Synergistic stimulation of human monocytes and dendritic cells by Toll-like receptor 4 and NOD1- and NOD2-activating agonists. Eur J Immunol 35(8):2459–2470PubMedCrossRef
38.
Zurück zum Zitat Li J et al (2004) Regulation of IL-8 and IL-1beta expression in Crohn’s disease associated NOD2/CARD15 mutations. Hum Mol Genet 13(16):1715–1725PubMedCrossRef Li J et al (2004) Regulation of IL-8 and IL-1beta expression in Crohn’s disease associated NOD2/CARD15 mutations. Hum Mol Genet 13(16):1715–1725PubMedCrossRef
39.
Zurück zum Zitat van Heel DA et al (2005) Synergistic enhancement of Toll-like receptor responses by NOD1 activation. Eur J Immunol 35(8):2471–2476PubMedCrossRef van Heel DA et al (2005) Synergistic enhancement of Toll-like receptor responses by NOD1 activation. Eur J Immunol 35(8):2471–2476PubMedCrossRef
40.
Zurück zum Zitat van Heel DA et al (2005) Muramyl dipeptide and toll-like receptor sensitivity in NOD2-associated Crohn’s disease. Lancet 365(9473):1794–1796PubMedCrossRef van Heel DA et al (2005) Muramyl dipeptide and toll-like receptor sensitivity in NOD2-associated Crohn’s disease. Lancet 365(9473):1794–1796PubMedCrossRef
41.
Zurück zum Zitat van Heel DA et al (2005) Synergy between TLR9 and NOD2 innate immune responses is lost in genetic Crohn’s disease. Gut 54(11):1553–1557PubMedCrossRef van Heel DA et al (2005) Synergy between TLR9 and NOD2 innate immune responses is lost in genetic Crohn’s disease. Gut 54(11):1553–1557PubMedCrossRef
42.
Zurück zum Zitat Uehara A et al (2005) Muramyldipeptide and diaminopimelic acid-containing desmuramylpeptides in combination with chemically synthesized Toll-like receptor agonists synergistically induced production of interleukin-8 in a NOD2- and NOD1-dependent manner, respectively, in human monocytic cells in culture. Cell Microbiol 7(1):53–61PubMedCrossRef Uehara A et al (2005) Muramyldipeptide and diaminopimelic acid-containing desmuramylpeptides in combination with chemically synthesized Toll-like receptor agonists synergistically induced production of interleukin-8 in a NOD2- and NOD1-dependent manner, respectively, in human monocytic cells in culture. Cell Microbiol 7(1):53–61PubMedCrossRef
43.
Zurück zum Zitat Tada H et al (2005) Synergistic effect of Nod1 and Nod2 agonists with toll-like receptor agonists on human dendritic cells to generate interleukin-12 and T helper type 1 cells. Infect Immun 73(12):7967–7976PubMedCrossRef Tada H et al (2005) Synergistic effect of Nod1 and Nod2 agonists with toll-like receptor agonists on human dendritic cells to generate interleukin-12 and T helper type 1 cells. Infect Immun 73(12):7967–7976PubMedCrossRef
44.
Zurück zum Zitat Ferwerda G et al (2005) NOD2 and toll-like receptors are nonredundant recognition systems of Mycobacterium tuberculosis. PLoS Pathog 1(3):279–285PubMedCrossRef Ferwerda G et al (2005) NOD2 and toll-like receptors are nonredundant recognition systems of Mycobacterium tuberculosis. PLoS Pathog 1(3):279–285PubMedCrossRef
45.
Zurück zum Zitat Watanabe H et al (2004) Innate immune response in Th1- and Th2-dominant mouse strains. Shock 22(5):460–466PubMedCrossRef Watanabe H et al (2004) Innate immune response in Th1- and Th2-dominant mouse strains. Shock 22(5):460–466PubMedCrossRef
46.
Zurück zum Zitat Rosenstiel P et al (2003) TNF-alpha and IFN-gamma regulate the expression of the NOD2 (CARD15) gene in human intestinal epithelial cells. Gastroenterology 124(4):1001–1009PubMedCrossRef Rosenstiel P et al (2003) TNF-alpha and IFN-gamma regulate the expression of the NOD2 (CARD15) gene in human intestinal epithelial cells. Gastroenterology 124(4):1001–1009PubMedCrossRef
47.
Zurück zum Zitat Takahashi Y et al (2006) Up-regulation of NOD1 and NOD2 through TLR4 and TNF-alpha in LPS-treated murine macrophages. J Vet Med Sci 68(5):471–478PubMedCrossRef Takahashi Y et al (2006) Up-regulation of NOD1 and NOD2 through TLR4 and TNF-alpha in LPS-treated murine macrophages. J Vet Med Sci 68(5):471–478PubMedCrossRef
48.
Zurück zum Zitat Chen CM et al (2004) Reciprocal cross-talk between Nod2 and TAK1 signaling pathways. J Biol Chem 279(24):25876–25882PubMedCrossRef Chen CM et al (2004) Reciprocal cross-talk between Nod2 and TAK1 signaling pathways. J Biol Chem 279(24):25876–25882PubMedCrossRef
49.
Zurück zum Zitat Kufer TA, Sansonetti PJ (2007) Sensing of bacteria: NOD a lonely job. Curr Opin Microbiol 10(1):62–69PubMedCrossRef Kufer TA, Sansonetti PJ (2007) Sensing of bacteria: NOD a lonely job. Curr Opin Microbiol 10(1):62–69PubMedCrossRef
50.
Zurück zum Zitat Chin AI et al (2002) Involvement of receptor-interacting protein 2 in innate and adaptive immune responses. Nature 416(6877):190–194PubMedCrossRef Chin AI et al (2002) Involvement of receptor-interacting protein 2 in innate and adaptive immune responses. Nature 416(6877):190–194PubMedCrossRef
51.
Zurück zum Zitat Kobayashi K et al (2002) RICK/Rip2/CARDIAK mediates signalling for receptors of the innate and adaptive immune systems. Nature 416(6877):194–199PubMedCrossRef Kobayashi K et al (2002) RICK/Rip2/CARDIAK mediates signalling for receptors of the innate and adaptive immune systems. Nature 416(6877):194–199PubMedCrossRef
52.
Zurück zum Zitat Lu C et al (2005) Participation of Rip2 in lipopolysaccharide signaling is independent of its kinase activity. J Biol Chem 280(16):16278–16283PubMedCrossRef Lu C et al (2005) Participation of Rip2 in lipopolysaccharide signaling is independent of its kinase activity. J Biol Chem 280(16):16278–16283PubMedCrossRef
53.
Zurück zum Zitat Mariathasan S, Monack DM (2007) Inflammasome adaptors and sensors: intracellular regulators of infection and inflammation. Nat Rev Immunol 7(1):31–40PubMedCrossRef Mariathasan S, Monack DM (2007) Inflammasome adaptors and sensors: intracellular regulators of infection and inflammation. Nat Rev Immunol 7(1):31–40PubMedCrossRef
54.
Zurück zum Zitat Kahlenberg JM et al (2005) Potentiation of caspase-1 activation by the P2X7 receptor is dependent on TLR signals and requires NF-kappaB-driven protein synthesis. J Immunol 175(11):7611–7622PubMed Kahlenberg JM et al (2005) Potentiation of caspase-1 activation by the P2X7 receptor is dependent on TLR signals and requires NF-kappaB-driven protein synthesis. J Immunol 175(11):7611–7622PubMed
55.
Zurück zum Zitat Pelegrin P, Surprenant A (2006) Pannexin-1 mediates large pore formation and interleukin-1beta release by the ATP-gated P2X7 receptor. EMBO J 25(21):5071–5082PubMedCrossRef Pelegrin P, Surprenant A (2006) Pannexin-1 mediates large pore formation and interleukin-1beta release by the ATP-gated P2X7 receptor. EMBO J 25(21):5071–5082PubMedCrossRef
56.
Zurück zum Zitat Solle M et al (2001) Altered cytokine production in mice lacking P2X(7) receptors. J Biol Chem 276(1):125–132PubMedCrossRef Solle M et al (2001) Altered cytokine production in mice lacking P2X(7) receptors. J Biol Chem 276(1):125–132PubMedCrossRef
57.
Zurück zum Zitat Miao EA et al (2006) Cytoplasmic flagellin activates caspase-1 and secretion of interleukin 1beta via Ipaf. Nat Immunol 7(6):569–575PubMedCrossRef Miao EA et al (2006) Cytoplasmic flagellin activates caspase-1 and secretion of interleukin 1beta via Ipaf. Nat Immunol 7(6):569–575PubMedCrossRef
58.
Zurück zum Zitat Miggin SM et al (2007) NF-kappaB activation by the Toll-IL-1 receptor domain protein MyD88 adapter-like is regulated by caspase-1. Proc Natl Acad Sci U S A 104(9):3372–3377PubMedCrossRef Miggin SM et al (2007) NF-kappaB activation by the Toll-IL-1 receptor domain protein MyD88 adapter-like is regulated by caspase-1. Proc Natl Acad Sci U S A 104(9):3372–3377PubMedCrossRef
59.
Zurück zum Zitat Grenier JM et al (2002) Functional screening of five PYPAF family members identifies PYPAF5 as a novel regulator of NF-kappaB and caspase-1. FEBS Lett 530(1–3):73–78PubMedCrossRef Grenier JM et al (2002) Functional screening of five PYPAF family members identifies PYPAF5 as a novel regulator of NF-kappaB and caspase-1. FEBS Lett 530(1–3):73–78PubMedCrossRef
60.
Zurück zum Zitat Wang L (2002) PYPAF7, a novel PYRIN-containing Apaf1-like protein that regulates activation of NF-kappa B and caspase-1-dependent cytokine processing. J Biol Chem 277(33):29874–29880PubMedCrossRef Wang L (2002) PYPAF7, a novel PYRIN-containing Apaf1-like protein that regulates activation of NF-kappa B and caspase-1-dependent cytokine processing. J Biol Chem 277(33):29874–29880PubMedCrossRef
61.
Zurück zum Zitat O’Connor W Jr et al (2003) Cutting edge: CIAS1/cryopyrin/PYPAF1/NALP3/CATERPILLER 1.1 is an inducible inflammatory mediator with NF-kappa B suppressive properties. J Immunol 171(12):6329–6333PubMed O’Connor W Jr et al (2003) Cutting edge: CIAS1/cryopyrin/PYPAF1/NALP3/CATERPILLER 1.1 is an inducible inflammatory mediator with NF-kappa B suppressive properties. J Immunol 171(12):6329–6333PubMed
62.
Zurück zum Zitat Williams KL et al (2005) The CATERPILLER protein monarch-1 is an antagonist of toll-like receptor-, tumor necrosis factor alpha-, and Mycobacterium tuberculosis-induced pro-inflammatory signals. J Biol Chem 280(48):39914–39924PubMedCrossRef Williams KL et al (2005) The CATERPILLER protein monarch-1 is an antagonist of toll-like receptor-, tumor necrosis factor alpha-, and Mycobacterium tuberculosis-induced pro-inflammatory signals. J Biol Chem 280(48):39914–39924PubMedCrossRef
63.
Zurück zum Zitat Franchi L et al (2006) Cytosolic flagellin requires Ipaf for activation of caspase-1 and interleukin 1beta in salmonella-infected macrophages. Nat Immunol 7(6):576–582PubMedCrossRef Franchi L et al (2006) Cytosolic flagellin requires Ipaf for activation of caspase-1 and interleukin 1beta in salmonella-infected macrophages. Nat Immunol 7(6):576–582PubMedCrossRef
64.
Zurück zum Zitat Berdeli A et al (2005) TLR-2 gene Arg753Gln polymorphism is strongly associated with acute rheumatic fever in children. J Mol Med 83(7):535–541PubMedCrossRef Berdeli A et al (2005) TLR-2 gene Arg753Gln polymorphism is strongly associated with acute rheumatic fever in children. J Mol Med 83(7):535–541PubMedCrossRef
65.
Zurück zum Zitat Ogus AC et al (2004) The Arg753GLn polymorphism of the human toll-like receptor 2 gene in tuberculosis disease. Eur Respir J 23(2):219–223PubMedCrossRef Ogus AC et al (2004) The Arg753GLn polymorphism of the human toll-like receptor 2 gene in tuberculosis disease. Eur Respir J 23(2):219–223PubMedCrossRef
66.
Zurück zum Zitat Moore CE et al (2004) Lack of association between Toll-like receptor 2 polymorphisms and susceptibility to severe disease caused by Staphylococcus aureus. Clin Diagn Lab Immunol 11(6):1194–1197PubMedCrossRef Moore CE et al (2004) Lack of association between Toll-like receptor 2 polymorphisms and susceptibility to severe disease caused by Staphylococcus aureus. Clin Diagn Lab Immunol 11(6):1194–1197PubMedCrossRef
67.
Zurück zum Zitat Kang TJ, Chae GT (2001) Detection of Toll-like receptor 2 (TLR2) mutation in the lepromatous leprosy patients. FEMS Immunol Med Microbiol 31(1):53–58PubMedCrossRef Kang TJ, Chae GT (2001) Detection of Toll-like receptor 2 (TLR2) mutation in the lepromatous leprosy patients. FEMS Immunol Med Microbiol 31(1):53–58PubMedCrossRef
68.
Zurück zum Zitat Agnese DM et al (2002) Human toll-like receptor 4 mutations but not CD14 polymorphisms are associated with an increased risk of gram-negative infections. J Infect Dis 186(10):1522–1525PubMedCrossRef Agnese DM et al (2002) Human toll-like receptor 4 mutations but not CD14 polymorphisms are associated with an increased risk of gram-negative infections. J Infect Dis 186(10):1522–1525PubMedCrossRef
69.
Zurück zum Zitat Child NJ et al (2003) Polymorphisms in Toll-like receptor 4 and the systemic inflammatory response syndrome. Biochem Soc Trans 31(Pt 3):652–653PubMedCrossRef Child NJ et al (2003) Polymorphisms in Toll-like receptor 4 and the systemic inflammatory response syndrome. Biochem Soc Trans 31(Pt 3):652–653PubMedCrossRef
70.
Zurück zum Zitat Minoretti P et al (2006) Effect of the functional toll-like receptor 4 Asp299Gly polymorphism on susceptibility to late-onset Alzheimer’s disease. Neurosci Lett 391(3):147–149PubMedCrossRef Minoretti P et al (2006) Effect of the functional toll-like receptor 4 Asp299Gly polymorphism on susceptibility to late-onset Alzheimer’s disease. Neurosci Lett 391(3):147–149PubMedCrossRef
71.
Zurück zum Zitat Zheng SL et al (2004) Sequence variants of toll-like receptor 4 are associated with prostate cancer risk: results from the CAncer Prostate in Sweden Study. Cancer Res 64(8):2918–2922PubMedCrossRef Zheng SL et al (2004) Sequence variants of toll-like receptor 4 are associated with prostate cancer risk: results from the CAncer Prostate in Sweden Study. Cancer Res 64(8):2918–2922PubMedCrossRef
72.
Zurück zum Zitat Hawn TR et al (2003) A common dominant TLR5 stop codon polymorphism abolishes flagellin signaling and is associated with susceptibility to legionnaires’ disease. J Exp Med 198(10):1563–1572PubMedCrossRef Hawn TR et al (2003) A common dominant TLR5 stop codon polymorphism abolishes flagellin signaling and is associated with susceptibility to legionnaires’ disease. J Exp Med 198(10):1563–1572PubMedCrossRef
73.
Zurück zum Zitat Tantisira K et al (2004) Toll-like receptor 6 gene (TLR6): single-nucleotide polymorphism frequencies and preliminary association with the diagnosis of asthma. Genes Immun 5(5):343–346PubMedCrossRef Tantisira K et al (2004) Toll-like receptor 6 gene (TLR6): single-nucleotide polymorphism frequencies and preliminary association with the diagnosis of asthma. Genes Immun 5(5):343–346PubMedCrossRef
74.
75.
Zurück zum Zitat Ku CL et al (2005) Inherited disorders of human Toll-like receptor signaling: immunological implications. Immunol Rev 203:10–20PubMedCrossRef Ku CL et al (2005) Inherited disorders of human Toll-like receptor signaling: immunological implications. Immunol Rev 203:10–20PubMedCrossRef
76.
Zurück zum Zitat Picard C et al (2003) Pyogenic bacterial infections in humans with IRAK-4 deficiency. Science 299(5615):2076–2079PubMedCrossRef Picard C et al (2003) Pyogenic bacterial infections in humans with IRAK-4 deficiency. Science 299(5615):2076–2079PubMedCrossRef
77.
Zurück zum Zitat Medvedev AE et al (2002) Dysregulation of LPS-induced Toll-like receptor 4-MyD88 complex formation and IL-1 receptor-associated kinase 1 activation in endotoxin-tolerant cells. J Immunol 169(9):5209–5216PubMed Medvedev AE et al (2002) Dysregulation of LPS-induced Toll-like receptor 4-MyD88 complex formation and IL-1 receptor-associated kinase 1 activation in endotoxin-tolerant cells. J Immunol 169(9):5209–5216PubMed
78.
Zurück zum Zitat Jefferies CA, O’Neill LA (2004) Bruton’s tyrosine kinase (Btk)-the critical tyrosine kinase in LPS signalling? Immunol Lett 92(1–2):15–22PubMedCrossRef Jefferies CA, O’Neill LA (2004) Bruton’s tyrosine kinase (Btk)-the critical tyrosine kinase in LPS signalling? Immunol Lett 92(1–2):15–22PubMedCrossRef
79.
Zurück zum Zitat Khor CC et al (2007) A Mal functional variant is associated with protection against invasive pneumococcal disease, bacteremia, malaria and tuberculosis. Nat Genet 39(4):523–528PubMedCrossRef Khor CC et al (2007) A Mal functional variant is associated with protection against invasive pneumococcal disease, bacteremia, malaria and tuberculosis. Nat Genet 39(4):523–528PubMedCrossRef
80.
Zurück zum Zitat Kiechl S et al (2002) Toll-like receptor 4 polymorphisms and atherogenesis. N Engl J Med 347(3):185–192PubMedCrossRef Kiechl S et al (2002) Toll-like receptor 4 polymorphisms and atherogenesis. N Engl J Med 347(3):185–192PubMedCrossRef
81.
Zurück zum Zitat Palmer SM et al (2003) The role of innate immunity in acute allograft rejection after lung transplantation. Am J Respir Crit Care Med 168(6):628–632PubMedCrossRef Palmer SM et al (2003) The role of innate immunity in acute allograft rejection after lung transplantation. Am J Respir Crit Care Med 168(6):628–632PubMedCrossRef
82.
Zurück zum Zitat Rudofsky G Jr et al (2004) Asp299Gly and Thr399Ile genotypes of the TLR4 gene are associated with a reduced prevalence of diabetic neuropathy in patients with type 2 diabetes. Diabetes Care 27(1):179–183PubMedCrossRef Rudofsky G Jr et al (2004) Asp299Gly and Thr399Ile genotypes of the TLR4 gene are associated with a reduced prevalence of diabetic neuropathy in patients with type 2 diabetes. Diabetes Care 27(1):179–183PubMedCrossRef
83.
Zurück zum Zitat Andersen-Nissen E et al (2005) Evasion of Toll-like receptor 5 by flagellated bacteria. Proc Natl Acad Sci U S A 102(26):9247–9252PubMedCrossRef Andersen-Nissen E et al (2005) Evasion of Toll-like receptor 5 by flagellated bacteria. Proc Natl Acad Sci U S A 102(26):9247–9252PubMedCrossRef
84.
Zurück zum Zitat Andersen-Nissen E et al (2007) A conserved surface on Toll-like receptor 5 recognizes bacterial flagellin. J Exp Med 204(2):393–403PubMedCrossRef Andersen-Nissen E et al (2007) A conserved surface on Toll-like receptor 5 recognizes bacterial flagellin. J Exp Med 204(2):393–403PubMedCrossRef
85.
Zurück zum Zitat Fortune SM et al (2004) Mycobacterium tuberculosis inhibits macrophage responses to IFN-gamma through myeloid differentiation factor 88-dependent and -independent mechanisms. J Immunol 172(10):6272–6280PubMed Fortune SM et al (2004) Mycobacterium tuberculosis inhibits macrophage responses to IFN-gamma through myeloid differentiation factor 88-dependent and -independent mechanisms. J Immunol 172(10):6272–6280PubMed
86.
Zurück zum Zitat Rosenstiel P, Till A, Schreiber S (2007) NOD-like receptors and human diseases. Microbes Infect 9(5):648–657PubMedCrossRef Rosenstiel P, Till A, Schreiber S (2007) NOD-like receptors and human diseases. Microbes Infect 9(5):648–657PubMedCrossRef
87.
Zurück zum Zitat Dinarello CA (1996) Biologic basis for interleukin-1 in disease. Blood 87(6):2095–2147PubMed Dinarello CA (1996) Biologic basis for interleukin-1 in disease. Blood 87(6):2095–2147PubMed
88.
Zurück zum Zitat Cook DN, Pisetsky DS, Schwartz DA (2004) Toll-like receptors in the pathogenesis of human disease. Nat Immunol 5(10):975–979PubMedCrossRef Cook DN, Pisetsky DS, Schwartz DA (2004) Toll-like receptors in the pathogenesis of human disease. Nat Immunol 5(10):975–979PubMedCrossRef
89.
Zurück zum Zitat Trinchieri G, Sher A (2007) Cooperation of Toll-like receptor signals in innate immune defence. Nat Rev Immunol 7(3):179–190PubMedCrossRef Trinchieri G, Sher A (2007) Cooperation of Toll-like receptor signals in innate immune defence. Nat Rev Immunol 7(3):179–190PubMedCrossRef
Metadaten
Titel
Inflammasomes in inflammatory disorders: the role of TLRs and their interactions with NLRs
verfasst von
Christine E. Becker
Luke A. J. O’Neill
Publikationsdatum
01.09.2007
Verlag
Springer-Verlag
Erschienen in
Seminars in Immunopathology / Ausgabe 3/2007
Print ISSN: 1863-2297
Elektronische ISSN: 1863-2300
DOI
https://doi.org/10.1007/s00281-007-0081-4

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