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PMID: 15481153
TLR4 is a receptor for Gram- LPS, Respiratory syncytial virus protein F, and other endogenous ligands, such as surfactant protein A and fibronectin fragment.</csml:comment>
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PMID: 15481153, 14620134, 12960260
TLR belong to a family of PRR that are used to recognize microbial products derived from several classes of microbes, as well as endogenous ligands that represent ‘‘danger signal’’.</csml:comment>
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<csml:comment type="text">




PMID: 15481153
TLR also contain a highly conserved cytoplasmic Toll-IL-1 receptor (TIR) domain that, through the adaptor molecule MyD88, connects the receptor to the intracellular signaling machinery shared by IL-1 and IL-18.</csml:comment>
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<csml:comment type="text">




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<csml:comment type="text">





PMID: 15481153
TLR3 mediates responses to viral dsRNA.</csml:comment>
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PMID: 15481153
This molecule links all TLR, with the possible exception of TLR3, to the complex IRAK1/4- TRAF6, which then leads to the activation of canonical NF-kappaB and MAPKs.</csml:comment>
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<csml:comment type="text">





PMID: 15481153
TLR2, in combination with either TLR1 or TLR6, recognizes several products including peptidoglycan, bacterial lipopeptides, mycobacterial lipoarabinomannan, and yeast zymosan.</csml:comment>
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<csml:comment type="text">





PMID: 15481153
TLR2, in combination with either TLR1 or TLR6, recognizes several products including peptidoglycan, bacterial lipopeptides, mycobacterial lipoarabinomannan, and yeast zymosan.</csml:comment>
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PMID: 15481153
TLR2, in combination with either TLR1 or TLR6, recognizes several products including peptidoglycan, bacterial lipopeptides, mycobacterial lipoarabinomannan, and yeast zymosan.</csml:comment>
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PMID: 15481153, 12539043, 12855817, 12692549
This pathway relies on a third adaptor called TRIF/TICAM (Oshiumi et al., 2003; Yamamoto et al., 2003a) that links TLR3 and TLR4 to the kinase complex IKKepsilon/TBK1, which in turn activates the transcription factor IRF3.</csml:comment>
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PMID: 15481153
TLR2, in combination with either TLR1 or TLR6, recognizes several products including peptidoglycan, bacterial lipopeptides, mycobacterial lipoarabinomannan, and yeast zymosan.</csml:comment>
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PMID: 15481153
TLR4 is a receptor for Gram- LPS, Respiratory syncytial virus protein F, and other endogenous ligands, such as surfactant protein A and fibronectin fragment.</csml:comment>
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<csml:comment type="text">




PMID: 15481153
TLR4 is a receptor for Gram- LPS, Respiratory syncytial virus protein F, and other endogenous ligands, such as surfactant protein A and fibronectin fragment.</csml:comment>
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PMID: 15481153
TLR4 is a receptor for Gram- LPS, Respiratory syncytial virus protein F, and other endogenous ligands, such as surfactant protein A and fibronectin fragment.</csml:comment>
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PMID: 15481153
TLR5 recognizes bacterial flagellin.</csml:comment>
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PMID: 15481153
TLR7 and TLR8 are receptors for ssRNA found in endosomal compartments and antiviral imidazoquinoline drugs that are structural mimetics of ssRNA.</csml:comment>
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PMID: 15481153
TLR7 and TLR8 are receptors for ssRNA found in endosomal compartments and antiviral imidazoquinoline drugs that are structural mimetics of ssRNA.</csml:comment>
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PMID: 15481153
TLR7 and TLR8 are receptors for ssRNA found in endosomal compartments and antiviral imidazoquinoline drugs that are structural mimetics of ssRNA.</csml:comment>
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PMID: 15481153
TLR7 and TLR8 are receptors for ssRNA found in endosomal compartments and antiviral imidazoquinoline drugs that are structural mimetics of ssRNA.</csml:comment>
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PMID: 15481153
TLR9 mediates responses to bacterial CpG DNA.</csml:comment>
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PMID: 15481153, 15001781
TLR11 mediates response to uropathogenic bacteria, although the nature of the agonist has not been identified.</csml:comment>
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<csml:comment type="text">




PMID: 15481153
This molecule links all TLR, with the possible exception of TLR3, to the complex IRAK1/4- TRAF6, which then leads to the activation of canonical NF-kappaB and MAPKs.</csml:comment>
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PMID: 15481153
This molecule links all TLR, with the possible exception of TLR3, to the complex IRAK1/4- TRAF6, which then leads to the activation of canonical NF-kappaB and MAPKs.</csml:comment>
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PMID: 15481153
This molecule links all TLR, with the possible exception of TLR3, to the complex IRAK1/4- TRAF6, which then leads to the activation of canonical NF-kappaB and MAPKs.</csml:comment>
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PMID: 15481153
The fact that different TLR can induce such an array of responses suggest that they possess the ability to selectively activate distinct signaling pathways, which include the MAP kinases p38, c-Jun N-terminal kinase, ERK1/2, the transcription factors NF-kappaB and IRF-3, the PI3 kinase, and caspase-1.</csml:comment>
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PMID: 15481153
The fact that different TLR can induce such an array of responses suggest that they possess the ability to selectively activate distinct signaling pathways, which include the MAP kinases p38, c-Jun N-terminal kinase, ERK1/2, the transcription factors NF-kappaB and IRF-3, the PI3 kinase, and caspase-1.</csml:comment>
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PMID: 15481153
The fact that different TLR can induce such an array of responses suggest that they possess the ability to selectively activate distinct signaling pathways, which include the MAP kinases p38, c-Jun N-terminal kinase, ERK1/2, the transcription factors NF-kappaB and IRF-3, the PI3 kinase, and caspase-1.</csml:comment>
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Indirect</csml:comment>
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<csml:comments>
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PMID: 15481153
The fact that different TLR can induce such an array of responses suggest that they possess the ability to selectively activate distinct signaling pathways, which include the MAP kinases p38, c-Jun N-terminal kinase, ERK1/2, the transcription factors NF-kappaB and IRF-3, the PI3 kinase, and caspase-1.</csml:comment>
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PMID: 15481153, 11544529, 11526399
The activation of this pathway by TLR2 and TLR4 is dependent on an additional TIR-containing adaptor called TIRAP/MALthat works in conjunction with MyD88.</csml:comment>
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<csml:comment type="text">



PMID: 15481153, 11544529, 11526399
The activation of this pathway by TLR2 and TLR4 is dependent on an additional TIR-containing adaptor called TIRAP/MALthat works in conjunction with MyD88.</csml:comment>
</csml:comments>
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<csml:comment type="text">



PMID: 15481153, 11544529, 11526399
The activation of this pathway by TLR2 and TLR4 is dependent on an additional TIR-containing adaptor called TIRAP/MALthat works in conjunction with MyD88.</csml:comment>
</csml:comments>
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PMID: 15481153, 14556004
TRAM, the most recently characterized TIR-containing adaptor, also appears to be required for both MyD88-dependent and MyD88-independent responses induced by TLR4.</csml:comment>
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PMID: 15481153, 12539043, 12855817, 12692549
This pathway relies on a third adaptor called TRIF/TICAM (Oshiumi et al., 2003; Yamamoto et al., 2003a) that links TLR3 and TLR4 to the kinase complex IKKepsilon/TBK1, which in turn activates the transcription factor IRF3.</csml:comment>
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PMID: 15481153, 12539043, 12855817, 12692549
This pathway relies on a third adaptor called TRIF/TICAM (Oshiumi et al., 2003; Yamamoto et al., 2003a) that links TLR3 and TLR4 to the kinase complex IKKepsilon/TBK1, which in turn activates the transcription factor IRF3.</csml:comment>
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<csml:comment type="text">



PMID: 15481153, 12539043, 12855817, 12692549
This pathway relies on a third adaptor called TRIF/TICAM (Oshiumi et al., 2003; Yamamoto et al., 2003a) that links TLR3 and TLR4 to the kinase complex IKKepsilon/TBK1, which in turn activates the transcription factor IRF3.</csml:comment>
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<csml:comment type="text">


Indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">


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<csml:comment type="text">



PMID: 15481153, 12354379, 11698465
IRF3 is responsible for the induction of a group of genes specific for TLR3/4 stimulation, such as IFN-beta and IP-10.

PMID: 15481153
For example, in human DC TLR3 is able to induce IP-10 and IL-15 to similar levels as TLR4, yet it induces IFN-beta only very weakly.</csml:comment>
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Indirect</csml:comment>
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<csml:comment type="text">



PMID: 15481153, 12354379, 11698465
IRF3 is responsible for the induction of a group of genes specific for TLR3/4 stimulation, such as IFN-beta and IP-10.

PMID: 15481153
Thus, while TLR2 activation is unable to induce Th1-specific factors (IP-10, IFN-beta, IL-12, and IL-15), it is at the same time capable of blocking the induction of some of them (IL-12 and IP-10) by TLR4 and TLR3.

PMID: 15481153
For example, in human DC TLR3 is able to induce IP-10 and IL-15 to similar levels as TLR4, yet it induces IFN-beta only very weakly.</csml:comment>
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</csml:comment>
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<csml:comment type="text">



PMID: 15481153
Furthermore, TRIF is capable of leading to the activation of NF-kappaB and MAPKs, and appears to be the only adaptor used by TLR3.</csml:comment>
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<csml:comment type="text">



PMID: 15481153
Furthermore, TRIF is capable of leading to the activation of NF-kappaB and MAPKs, and appears to be the only adaptor used by TLR3.</csml:comment>
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Indirect</csml:comment>
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<csml:comment type="text">



PMID: 15481153
Furthermore, TRIF is capable of leading to the activation of NF-kappaB and MAPKs, and appears to be the only adaptor used by TLR3.</csml:comment>
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Indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
Furthermore, TRIF is capable of leading to the activation of NF-kappaB and MAPKs, and appears to be the only adaptor used by TLR3.</csml:comment>
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Indirect</csml:comment>
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<csml:comment type="text">



PMID: 15481153
TLR signaling initiates DC maturation, a differentiation process in which the antigen is captured and processed into peptides that are then presented in the context of MHC class II molecules.</csml:comment>
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Indirect</csml:comment>
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PMID: 15481153
Various TLR agonists activate mast cells, eosinophil, neutrophils, B cells, endothelial cells, and several types of epithelia, and regulate proliferation and apoptosis of different cell types.</csml:comment>
</csml:comments>
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Indirect</csml:comment>
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PMID: 15481153
Various TLR agonists activate mast cells, eosinophil, neutrophils, B cells, endothelial cells, and several types of epithelia, and regulate proliferation and apoptosis of different cell types.</csml:comment>
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PMID: 15481153
NF-kappaB and MAPK family members were activated to the same extent and with similar kinetics by both TLR2 and TLR4 agonists in the DC.</csml:comment>
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<csml:comment type="text">



PMID: 15481153
NF-kappaB and MAPK family members were activated to the same extent and with similar kinetics by both TLR2 and TLR4 agonists in the DC.</csml:comment>
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PMID: 15481153
NF-kappaB and MAPK family members were activated to the same extent and with similar kinetics by both TLR2 and TLR4 agonists in the DC.</csml:comment>
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PMID: 15481153
NF-kappaB and MAPK family members were activated to the same extent and with similar kinetics by both TLR2 and TLR4 agonists in the DC.</csml:comment>
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Indirect</csml:comment>
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PMID: 15481153
TLR2 and TLR4 agonists were also equally capable of inducing DC maturation as measured by the up-regulation of several cell surface markers such as CD40, CD86, HLA-DR, and CD83.</csml:comment>
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<csml:comment type="text">



PMID: 15481153
Among the several cytokines and chemokines that were analyzed, IL-12p70, IP-10, IFNb, and IL-15 expression was exclusively induced by the TLR4 agonist LPS and not by TLR2 agonists.

PMID: 15481153
IFN-beta, IFIT1, and ISG15 belong to the primary response group.</csml:comment>
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<csml:comment type="text">



PMID: 15481153
Among the several cytokines and chemokines that were analyzed, IL-12p70, IP-10, IFNb, and IL-15 expression was exclusively induced by the TLR4 agonist LPS and not by TLR2 agonists.

PMID: 15481153, 15001781
IP-10 also appears to be part of this group, although it has been suggested otherwise.

PMID: 15481153
Thus, while TLR2 activation is unable to induce Th1-specific factors (IP-10, IFN-beta, IL-12, and IL-15), it is at the same time capable of blocking the induction of some of them (IL-12 and IP-10) by TLR4 and TLR3.</csml:comment>
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PMID: 15481153
Among the several cytokines and chemokines that were analyzed, IL-12p70, IP-10, IFNb, and IL-15 expression was exclusively induced by the TLR4 agonist LPS and not by TLR2 agonists.

PMID: 15481153
Thus, while TLR2 activation is unable to induce Th1-specific factors (IP-10, IFN-beta, IL-12, and IL-15), it is at the same time capable of blocking the induction of some of them (IL-12 and IP-10) by TLR4 and TLR3.</csml:comment>
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PMID: 15481153
Among the several cytokines and chemokines that were analyzed, IL-12p70, IP-10, IFN-beta, and IL-15 expression was exclusively induced by the TLR4 agonist LPS and not by TLR2 agonists.

PMID: 15481153
It is currently unclear as to what group other TLR4-specific genes, such as IL12p35 and IL-15, belong to.</csml:comment>
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<csml:comment type="text">



PMID: 15481153
In contrast, TLR2 agonists preferentially induced IL-8, IL-10, and IL-23p19.</csml:comment>
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<csml:comment type="text">



PMID: 15481153
In contrast, TLR2 agonists preferentially induced IL-8, IL-10, and IL-23p19.</csml:comment>
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<csml:comment type="text">



PMID: 15481153
In contrast, TLR2 agonists preferentially induced IL-8, IL-10, and IL-23p19.</csml:comment>
</csml:comments>
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PMID: 15481153
The p40 subunit is expressed in large excess of the p35 subunit, which is the limiting factor in controlling IL-12p70 production.</csml:comment>
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PMID: 15481153
IL-12p40 can also form homodimers that act as IL-12 receptor antagonist, or can pair with p19 to form IL-23, a novel cytokine whose activities remain poorly characterized.</csml:comment>
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PMID: 15481153
IL-12p40 can also form homodimers that act as IL-12 receptor antagonist, or can pair with p19 to form IL-23, a novel cytokine whose activities remain poorly characterized.</csml:comment>
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<csml:comment type="text">



PMID: 15481153
IL-12p40 can also form homodimers that act as IL-12 receptor antagonist, or can pair with p19 to form IL-23, a novel cytokine whose activities remain poorly characterized.</csml:comment>
</csml:comments>
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Indirect</csml:comment>
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Indirect</csml:comment>
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<csml:comment type="text">


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<csml:comment type="text">



PMID: 15481153, 12563297
IL-12 is able to stimulate IFN-gamma production in T cells, and is the key cytokine that directs the development of human and murine Th1 cells.</csml:comment>
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Indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
The fact that TLR4, but not TLR2, is able to induce the p35 subunit of IL-12, suggests that the Th1/ Th2 balance may be directly affected by the action of TLR.

PMID: 15481153
It is currently unclear as to what group other TLR4-specific genes, such as IL12p35 and IL-15, belong to.</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


Indirect</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
</csml:comments>
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<csml:parameter key="coefficient1" value="0.1"/>
<csml:parameter key="coefficient2" value="1.0"/>
</csml:processKinetic>
</csml:processSimulationProperty>
<csml:viewProperty>
<csml:position position="auto" positionID="default" x="384.0" y="1112.0"/>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
It is remarkable that TLR2 stimulation, while failing to induce IL-12p70 release due to defective p35 gene induction, is nevertheless still able to stimulate.</csml:comment>
</csml:comments>
</csml:process>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
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<csml:comments>
<csml:comment type="text">


Indirect</csml:comment>
</csml:comments>
</csml:connector>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
</csml:comments>
</csml:connector>
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</csml:processKinetic>
</csml:processSimulationProperty>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
IP-10, a CXC chemokine produced by different cell types in response to IFN-gamma and microbial products, is a chemoattractant for monocytes, NK cells, and, importantly, Th1 cells that preferentially express the IP-10 receptor CXCR3.</csml:comment>
</csml:comments>
</csml:process>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
</csml:comments>
</csml:connector>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
</csml:comments>
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</csml:processKinetic>
</csml:processSimulationProperty>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
IL-15 is particularly active on NK cells and strongly induces IFN-gamma release by this cell type.</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


Indirect</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
</csml:comments>
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</csml:processKinetic>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
IFN-beta, IFIT1, and ISG15 belong to the primary response group.</csml:comment>
</csml:comments>
</csml:process>
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<csml:comments>
<csml:comment type="text">


Indirect</csml:comment>
</csml:comments>
</csml:connector>
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<csml:comment type="text">


</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
IFN-beta, IFIT1, and ISG15 belong to the primary response group.</csml:comment>
</csml:comments>
</csml:process>
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<csml:comments>
<csml:comment type="text">


Indirect</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
The secondary response group comprises interferon response genes, such as RF7, IRF9, and PKR.</csml:comment>
</csml:comments>
</csml:process>
<csml:process id="p78" name="p78" type="cso30:c:ProcessBiological">
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<csml:comments>
<csml:comment type="text">


Indirect</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
The secondary response group comprises interferon response genes, such as RF7, IRF9, and PKR.</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


Indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
The secondary response group comprises interferon response genes, such as RF7, IRF9, and PKR.</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


Indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
Finally, IFN-beta is a type I interferon that induces Th1 differentiation in humans.</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


Indirect</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
Stimulation with TLR4 agonist led to the production of IP-10, IFN-beta, MCP5, iNOS, and IL-12p40.</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


Indirect</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 15481153
Stimulation with TLR4 agonist led to the production of IP-10, IFN-beta, MCP5, iNOS, and IL-12p40.</csml:comment>
</csml:comments>
</csml:process>
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PMID: 15481153, 12766768
In murine B cells, CpG DNA (TLR9 agonist), but not LPS, was found to induce the transcription factor T-bet and inhibit IgG1 and IgE switching induced by IL-4.</csml:comment>
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Indirect</csml:comment>
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PMID: 15481153
Moreover, the Th2 cytokines IL-4 and IL-5 were more abundantly released by mast cells stimulated through TLR2 than TLR4.</csml:comment>
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PMID: 15481153
Moreover, the Th2 cytokines IL-4 and IL-5 were more abundantly released by mast cells stimulated through TLR2 than TLR4.</csml:comment>
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PMID: 15481153
Moreover, the Th2 cytokines IL-4 and IL-5 were more abundantly released by mast cells stimulated through TLR2 than TLR4.</csml:comment>
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<csml:comment type="text">



PMID: 15481153
Moreover, the Th2 cytokines IL-4 and IL-5 were more abundantly released by mast cells stimulated through TLR2 than TLR4.</csml:comment>
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Indirect</csml:comment>
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PMID: 15481153
Preincubation with TLR2 agonist also blocked the induction of IP-10 by IFN-beta, suggesting that the mechanism of inhibition is not specific for TLR, or due to rapid tolerization, but rather is more proximal and restricted to the transcription of those genes.</csml:comment>
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PMID: 15481153, 12045249
Plasmacytoid cells respond by producing IFN-alpha, while myeloid DC preferentially express IL-12.</csml:comment>
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PMID: 15481153, 12045249
Plasmacytoid cells respond by producing IFN-alpha, while myeloid DC preferentially express IL-12.</csml:comment>
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PMID: 15481153, 14607893, 14579266, 12761116
The ability of TLR2 and TLR4 to induce distinct Th responses was confirmed in humans by in vitro Th cell differentiation experiments, and found to mirror the results obtained in mice, such that TLR2 agonists induced Th2 diffrentiation and TLR4 induced Th1.</csml:comment>
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PMID: 15481153, 14607893, 14579266, 12761116
The ability of TLR2 and TLR4 to induce distinct Th responses was confirmed in humans by in vitro Th cell differentiation experiments, and found to mirror the results obtained in mice, such that TLR2 agonists induced Th2 diffrentiation and TLR4 induced Th1.</csml:comment>
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PMID: 15481153, 12045249, 11812998
Similarly, TLR7 can induce IFN-alpha in human plasmacytoid DC (Ito et al., 2002) despite its inability to activate MyD88-independent signaling pathways.</csml:comment>
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PMID: 15481153
For example, in human DC TLR3 is able to induce IP-10 and IL-15 to similar levels as TLR4, yet it induces IFN-beta only very weakly.</csml:comment>
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Indirect</csml:comment>
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PMID: 15481153, 11313410
DC maturation induced by LPS is a MyD88-independent response (Kaisho et al., 2001); however, it is also induced by TLR that cannot link to TRIF.</csml:comment>
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PMID: 15481153, 12356687
For example, although both TLR2 and TLR9 exclusively activate the MyD88-dependent pathway, only TLR9 is able to induce IFN-beta production in mouse macrophages (Hoshino et al., 2002), thereby indicating the existence of differences between TLR2 and TLR9 that are not ascribable to the TRIF/IRF3 pathway.</csml:comment>
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PMID: 15481153
TLR2 and TLR4 agonists were also equally capable of inducing DC maturation as measured by the up-regulation of several cell surface markers such as CD40, CD86, HLA-DR, and CD83.</csml:comment>
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<csml:comment type="text">

PMID: 15481153
TLR2 and TLR4 agonists were also equally capable of inducing DC maturation as measured by the up-regulation of several cell surface markers such as CD40, CD86, HLA-DR, and CD83.</csml:comment>
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PMID: 15481153
TLR2 and TLR4 agonists were also equally capable of inducing DC maturation as measured by the up-regulation of several cell surface markers such as CD40, CD86, HLA-DR, and CD83.</csml:comment>
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PMID: 15481153
The fact that different TLR can induce such an array of responses suggest that they possess the ability to selectively activate distinct signaling pathways, which include the MAP kinases p38, c-Jun N-terminal kinase, ERK1/2, the transcription factors NF-kappaB and IRF-3, the PI3 kinase, and caspase-1.</csml:comment>
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PMID: 15481153
The fact that different TLR can induce such an array of responses suggest that they possess the ability to selectively activate distinct signaling pathways, which include the MAP kinases p38, c-Jun N-terminal kinase, ERK1/2, the transcription factors NF-kappaB and IRF-3, the PI3 kinase, and caspase-1.</csml:comment>
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PMID: 15481153
The fact that different TLR can induce such an array of responses suggest that they possess the ability to selectively activate distinct signaling pathways, which include the MAP kinases p38, c-Jun N-terminal kinase, ERK1/2, the transcription factors NF-kappaB and IRF-3, the PI3 kinase, and caspase-1.</csml:comment>
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<csml:comment type="text">PMID: 15481153
Stimulation with TLR4 agonist led to the production of IP-10, IFN-beta, MCP5, iNOS, and IL-12p40.</csml:comment>
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