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As mentioned, several non-TLR receptor chains cooperate with TLRs for the recognition of PAMPs; examples are CD14 and CD11b/CD18 for recognition of LPS by TLR4 [17 ], CD14 for recognition of lipoteichoic acid by TLR4 [18 ], and dectin-1 for recognition of zymosan and Candida albicans by TLR2 [19 , 20 ].</csml:comment>
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<csml:comment type="text">PMID: 15075354, 12072369, 7500012, 12719478, 12719479
As mentioned, several non-TLR receptor chains cooperate with TLRs for the recognition of PAMPs; examples are CD14 and CD11b/CD18 for recognition of LPS by TLR4 [17 ], CD14 for recognition of lipoteichoic acid by TLR4 [18 ], and dectin-1 for recognition of zymosan and Candida albicans by TLR2 [19 , 20 ].</csml:comment>
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As mentioned, several non-TLR receptor chains cooperate with TLRs for the recognition of PAMPs; examples are CD14 and CD11b/CD18 for recognition of LPS by TLR4 [17 ], CD14 for recognition of lipoteichoic acid by TLR4 [18 ], and dectin-1 for recognition of zymosan and Candida albicans by TLR2 [19 , 20 ].</csml:comment>
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<csml:comment type="text">PMID: 15075354, 12072369, 7500012, 12719478, 12719479
As mentioned, several non-TLR receptor chains cooperate with TLRs for the recognition of PAMPs; examples are CD14 and CD11b/CD18 for recognition of LPS by TLR4 [17 ], CD14 for recognition of lipoteichoic acid by TLR4 [18 ], and dectin-1 for recognition of zymosan and Candida albicans by TLR2 [19 , 20 ].</csml:comment>
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<csml:comment type="text">PMID: 15075354, 12072369, 7500012, 12719478, 12719479
As mentioned, several non-TLR receptor chains cooperate with TLRs for the recognition of PAMPs; examples are CD14 and CD11b/CD18 for recognition of LPS by TLR4 [17 ], CD14 for recognition of lipoteichoic acid by TLR4 [18 ], and dectin-1 for recognition of zymosan and Candida albicans by TLR2 [19 , 20 ].</csml:comment>
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As mentioned, several non-TLR receptor chains cooperate with TLRs for the recognition of PAMPs; examples are CD14 and CD11b/CD18 for recognition of LPS by TLR4 [17 ], CD14 for recognition of lipoteichoic acid by TLR4 [18 ], and dectin-1 for recognition of zymosan and Candida albicans by TLR2 [19 , 20 ].</csml:comment>
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As mentioned, several non-TLR receptor chains cooperate with TLRs for the recognition of PAMPs; examples are CD14 and CD11b/CD18 for recognition of LPS by TLR4 [17 ], CD14 for recognition of lipoteichoic acid by TLR4 [18 ], and dectin-1 for recognition of zymosan and Candida albicans by TLR2 [19 , 20 ].</csml:comment>
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As mentioned, several non-TLR receptor chains cooperate with TLRs for the recognition of PAMPs; examples are CD14 and CD11b/CD18 for recognition of LPS by TLR4 [17 ], CD14 for recognition of lipoteichoic acid by TLR4 [18 ], and dectin-1 for recognition of zymosan and Candida albicans by TLR2 [19 , 20 ].</csml:comment>
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<csml:comment type="text">PMID: 15075354, 12527213
The specificity of TLR recognition for several important PAMPs has been identified, including recognition of peptidoglycan (PGN), bacterial lipoproteins, and zymosan by TLR2; double-stranded RNA by TLR3; lipopolysaccharide (LPS) and heat-shock proteins (HSPs) by TLR4; flagellin by TLR5; and CpG motifs of bacterial DNA by TLR9 [5 ].</csml:comment>
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<csml:comment type="text">PMID: 15075354, 12527213
The specificity of TLR recognition for several important PAMPs has been identified, including recognition of peptidoglycan (PGN), bacterial lipoproteins, and zymosan by TLR2; double-stranded RNA by TLR3; lipopolysaccharide (LPS) and heat-shock proteins (HSPs) by TLR4; flagellin by TLR5; and CpG motifs of bacterial DNA by TLR9 [5 ].</csml:comment>
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The specificity of TLR recognition for several important PAMPs has been identified, including recognition of peptidoglycan (PGN), bacterial lipoproteins, and zymosan by TLR2; double-stranded RNA by TLR3; lipopolysaccharide (LPS) and heat-shock proteins (HSPs) by TLR4; flagellin by TLR5; and CpG motifs of bacterial DNA by TLR9 [5 ].</csml:comment>
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The specificity of TLR recognition for several important PAMPs has been identified, including recognition of peptidoglycan (PGN), bacterial lipoproteins, and zymosan by TLR2; double-stranded RNA by TLR3; lipopolysaccharide (LPS) and heat-shock proteins (HSPs) by TLR4; flagellin by TLR5; and CpG motifs of bacterial DNA by TLR9 [5 ].</csml:comment>
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The specificity of TLR recognition for several important PAMPs has been identified, including recognition of peptidoglycan (PGN), bacterial lipoproteins, and zymosan by TLR2; double-stranded RNA by TLR3; lipopolysaccharide (LPS) and heat-shock proteins (HSPs) by TLR4; flagellin by TLR5; and CpG motifs of bacterial DNA by TLR9 [5 ].</csml:comment>
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The specificity of TLR recognition for several important PAMPs has been identified, including recognition of peptidoglycan (PGN), bacterial lipoproteins, and zymosan by TLR2; double-stranded RNA by TLR3; lipopolysaccharide (LPS) and heat-shock proteins (HSPs) by TLR4; flagellin by TLR5; and CpG motifs of bacterial DNA by TLR9 [5 ].</csml:comment>
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The TLR–PAMP interaction results in the recruitment of specific adaptor molecules such as MyD88 and Mal, which then bind the IL-1R-associated kinase (IRAK).</csml:comment>
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The TLR–PAMP interaction results in the recruitment of specific adaptor molecules such as MyD88 and Mal, which then bind the IL-1R-associated kinase (IRAK).</csml:comment>
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The TLR–PAMP interaction results in the recruitment of specific adaptor molecules such as MyD88 and Mal, which then bind the IL-1R-associated kinase (IRAK).</csml:comment>
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The signal is thereafter transmitted through a chain of signaling molecules, which is apparently common to all TLRs, involving the tumor necrosis factor (TNF) receptor-associated factor-6 (TRAF6) and mitogen-activated protein kinases.</csml:comment>
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The signal is thereafter transmitted through a chain of signaling molecules, which is apparently common to all TLRs, involving the tumor necrosis factor (TNF) receptor-associated factor-6 (TRAF6) and mitogen-activated protein kinases.</csml:comment>
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Thereafter, activation of nuclear factor NF-kappaB and activated protein-1 (AP-1) leads to transcription of genes involved in the activation of the innate host defense, notably proinflammatory cytokines.</csml:comment>
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Thereafter, activation of nuclear factor NF-kappaB and activated protein-1 (AP-1) leads to transcription of genes involved in the activation of the innate host defense, notably proinflammatory cytokines.</csml:comment>
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<csml:comment type="text">PMID: 15075354
Thereafter, activation of nuclear factor NF-kappaB and activated protein-1 (AP-1) leads to transcription of genes involved in the activation of the innate host defense, notably proinflammatory cytokines.</csml:comment>
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Thereafter, activation of nuclear factor NF-kappaB and activated protein-1 (AP-1) leads to transcription of genes involved in the activation of the innate host defense, notably proinflammatory cytokines.</csml:comment>
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<csml:comment type="text">PMID: 15075354, 14556004
Moreover, a recent study described TRAM as an adaptor molecule specifically recruited to TLR4.

PMID: 15075354
Ligation of TLR4 recruits TRIF and transverse rectus abdominis musculocutaneous (TRAM), mediating unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IP-10 and iNOS.</csml:comment>
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Ligation of TLR4 or TLR3 recruits an additional adaptor molecule called TIR domain-containing, adapter-inducing interferon-ß (IFN-beta; TRIF).</csml:comment>
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<csml:comment type="text">PMID: 15075354, 12855817, 12872135
Ligation of TLR4 or TLR3 recruits an additional adaptor molecule called TIR domain-containing, adapter-inducing interferon-ß (IFN-beta; TRIF).

PMID: 15075354
Ligation of TLR4 recruits TRIF and transverse rectus abdominis musculocutaneous (TRAM), mediating unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IP-10 and iNOS.</csml:comment>
</csml:comments>
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<csml:comment type="text">Indirect</csml:comment>
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<csml:comment type="text">PMID: 15075354
In addition to potentiating the secretion of the proinflammatory cytokines, TRIF mediates unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IFN-inducible protein 10 (IP-10) and inducible nitric oxide synthase (iNOS).

PMID: 15075354
Ligation of TLR4 recruits TRIF and transverse rectus abdominis musculocutaneous (TRAM), mediating unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IP-10 and iNOS.</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">PMID: 15075354
In addition to potentiating the secretion of the proinflammatory cytokines, TRIF mediates unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IFN-inducible protein 10 (IP-10) and inducible nitric oxide synthase (iNOS).</csml:comment>
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<csml:comment type="text">PMID: 15075354
In addition to potentiating the secretion of the proinflammatory cytokines, TRIF mediates unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IFN-inducible protein 10 (IP-10) and inducible nitric oxide synthase (iNOS).</csml:comment>
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<csml:comment type="text">PMID: 15075354
In addition to potentiating the secretion of the proinflammatory cytokines, TRIF mediates unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IFN-inducible protein 10 (IP-10) and inducible nitric oxide synthase (iNOS).

PMID: 15075354
Ligation of TLR4 recruits TRIF and transverse rectus abdominis musculocutaneous (TRAM), mediating unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IP-10 and iNOS.</csml:comment>
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In addition to potentiating the secretion of the proinflammatory cytokines, TRIF mediates unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IFN-inducible protein 10 (IP-10) and inducible nitric oxide synthase (iNOS).</csml:comment>
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In addition to potentiating the secretion of the proinflammatory cytokines, TRIF mediates unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IFN-inducible protein 10 (IP-10) and inducible nitric oxide synthase (iNOS).

PMID: 15075354
Ligation of TLR4 recruits TRIF and transverse rectus abdominis musculocutaneous (TRAM), mediating unique signals leading to secretion of IFN-beta and indirect up-regulation of IFN-dependent genes such as IP-10 and iNOS.</csml:comment>
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<csml:comment type="text">PMID: 15075354, 11431423
In this way, heterodimers of TLR2/TLR1 recognize triacetylated bacterial lipopeptides, whereas TLR2/TLR6 heterodimeres recognize diacetylated Mycoplasma lipopeptides [16 ], and similar heterodimerization is likely to occur for other PAMPs.</csml:comment>
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<csml:comment type="text">PMID: 15075354, 11431423
In this way, heterodimers of TLR2/TLR1 recognize triacetylated bacterial lipopeptides, whereas TLR2/TLR6 heterodimeres recognize diacetylated Mycoplasma lipopeptides [16 ], and similar heterodimerization is likely to occur for other PAMPs.</csml:comment>
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<csml:comment type="text">PMID: 15075354
Our recent finding that NOD2, an intracellular molecule involved in the pathogenesis of Crohn’s disease, specifically mediates cytokine induction by TLR2 but not TLR4 agonists indicates that it may be part of a TLR2-specific pathway.</csml:comment>
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TLR2 also mediates host defense against T. gondii by mediating cytokine and NO release.</csml:comment>
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MyD88 is essential for the stimulation of proinflammatory cytokines such as TNF, IL-1beta, IL-12, or IL-6, virtually by the entire range of TLR agonists.</csml:comment>
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MyD88 is essential for the stimulation of proinflammatory cytokines such as TNF, IL-1beta, IL-12, or IL-6, virtually by the entire range of TLR agonists.</csml:comment>
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MyD88 is essential for the stimulation of proinflammatory cytokines such as TNF, IL-1beta, IL-12, or IL-6, virtually by the entire range of TLR agonists.</csml:comment>
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MyD88 is essential for the stimulation of proinflammatory cytokines such as TNF, IL-1beta, IL-12, or IL-6, virtually by the entire range of TLR agonists.

PMID: 15075354, 12761116
The stimulation of specific TLRs results in the release of IL-10 or IL-12, leading to skewing of the T cell response toward Th1 or Th2 cytokines.</csml:comment>
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The protective mechanisms triggered through MyD88 mainly include release of proinflammatory cytokines and of reactive nitrogen and oxygen intermediates.</csml:comment>
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The protective mechanisms triggered through MyD88 mainly include release of proinflammatory cytokines and of reactive nitrogen and oxygen intermediates.</csml:comment>
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The protective mechanisms triggered through MyD88 mainly include release of proinflammatory cytokines and of reactive nitrogen and oxygen intermediates.</csml:comment>
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<csml:comment type="text">PMID: 15075354
Stimulation of immature DC by microbial stimuli induces production of proinflammatory cytokines such as TNF and IL-12, which can induce differentiation of T cells into T helper cell type 1 (Th1) cells.</csml:comment>
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<csml:comment type="text">PMID: 15075354
Stimulation of immature DC by microbial stimuli induces production of proinflammatory cytokines such as TNF and IL-12, which can induce differentiation of T cells into T helper cell type 1 (Th1) cells.</csml:comment>
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<csml:comment type="text">PMID: 15075354, 9521319
In addition, these stimuli induce up-regulation of costimulatory molecules such as CD40, CD80, and CD86.</csml:comment>
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In addition, these stimuli induce up-regulation of costimulatory molecules such as CD40, CD80, and CD86.</csml:comment>
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In addition, these stimuli induce up-regulation of costimulatory molecules such as CD40, CD80, and CD86.</csml:comment>
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<csml:comment type="text">PMID: 15075354, 11286707, 11561001
A variety of microbial PAMPs are able to induce cytokine release and DC maturation: LPS through TLR4, CpG through TLR9, bacterial lipopeptides through TLR2.</csml:comment>
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A variety of microbial PAMPs are able to induce cytokine release and DC maturation: LPS through TLR4, CpG through TLR9, bacterial lipopeptides through TLR2.</csml:comment>
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<csml:comment type="text">PMID: 15075354, 11286707, 11561001
A variety of microbial PAMPs are able to induce cytokine release and DC maturation: LPS through TLR4, CpG through TLR9, bacterial lipopeptides through TLR2.</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">PMID: 15075354, 11286707, 11561001
A variety of microbial PAMPs are able to induce cytokine release and DC maturation: LPS through TLR4, CpG through TLR9, bacterial lipopeptides through TLR2.</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">PMID: 15075354, 11286707, 11561001
A variety of microbial PAMPs are able to induce cytokine release and DC maturation: LPS through TLR4, CpG through TLR9, bacterial lipopeptides through TLR2.

PMID: 15075354, 11286707
One pathway induced mainly by TLR9 is strictly dependent on MyD88, whereas another pathway induced primarily by TLR4 can induce DC maturation through a MyD88-independent mechanism.</csml:comment>
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<csml:comment type="text">PMID: 15075354, 11286707, 11561001
A variety of microbial PAMPs are able to induce cytokine release and DC maturation: LPS through TLR4, CpG through TLR9, bacterial lipopeptides through TLR2.</csml:comment>
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<csml:comments>
<csml:comment type="text">PMID: 15075354
Thus, whereas interaction of Candida mannan with TLR4 induces release of chemokines, leukocyte recruitment, and protection, interaction of Candida glucans and phospholipomannan with TLR2 primarily mediates release of the anti-inflammatory cytokine IL-10, resulting in inhibition of the host defense and increased susceptibility to infection.</csml:comment>
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<csml:comments>
<csml:comment type="text">Indirect</csml:comment>
</csml:comments>
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<csml:parameter key="stoichiometry" value="1"/>
</csml:connectorKinetic>
</csml:connectorSimulationProperty>
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<csml:comments>
<csml:comment type="text">PMID: 15075354, 12761116
The stimulation of specific TLRs results in the release of IL-10 or IL-12, leading to skewing of the T cell response toward Th1 or Th2 cytokines.</csml:comment>
</csml:comments>
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<csml:comment type="text">Indirect</csml:comment>
</csml:comments>
</csml:connector>
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</csml:comments>
</csml:connector>
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<csml:comment type="text">PMID: 15075354, 12391013
Yersinia enterocolitica and C. albicans have been shown to exploit TLR2-mediated IL-10 release to induce immunosuppression.

PMID: 15075354
Thus, whereas interaction of Candida mannan with TLR4 induces release of chemokines, leukocyte recruitment, and protection, interaction of Candida glucans and phospholipomannan with TLR2 primarily mediates release of the anti-inflammatory cytokine IL-10, resulting in inhibition of the host defense and increased susceptibility to infection.</csml:comment>
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