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PMID: 18641647, 9237759, 11323673, 10364168
The leucine-rich repeats of the TLR ectodomains bind to pathogen-associated molecular patterns (PAMPs), such as the bacterial cell-wall component lipopolysaccharide (a ligand of TLR4), bacterial flagellin (a ligand of TLR5), and lipoprotein and peptidoglycan (which are recognized by TLR2 complexed with TLR1 or TLR6).</csml:comment>
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PMID: 18641647, 9237759, 11323673, 10364168
The leucine-rich repeats of the TLR ectodomains bind to pathogen-associated molecular patterns (PAMPs), such as the bacterial cell-wall component lipopolysaccharide (a ligand of TLR4), bacterial flagellin (a ligand of TLR5), and lipoprotein and peptidoglycan (which are recognized by TLR2 complexed with TLR1 or TLR6).</csml:comment>
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<csml:comments>
<csml:comment type="text">





PMID: 18641647, 9237759, 11323673, 10364168
The leucine-rich repeats of the TLR ectodomains bind to pathogen-associated molecular patterns (PAMPs), such as the bacterial cell-wall component lipopolysaccharide (a ligand of TLR4), bacterial flagellin (a ligand of TLR5), and lipoprotein and peptidoglycan (which are recognized by TLR2 complexed with TLR1 or TLR6).</csml:comment>
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<csml:comments>
<csml:comment type="text">





PMID: 18641647, 9237759, 11323673, 10364168
The leucine-rich repeats of the TLR ectodomains bind to pathogen-associated molecular patterns (PAMPs), such as the bacterial cell-wall component lipopolysaccharide (a ligand of TLR4), bacterial flagellin (a ligand of TLR5), and lipoprotein and peptidoglycan (which are recognized by TLR2 complexed with TLR1 or TLR6).</csml:comment>
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PMID: 18641647
TLR7 and TLR8 respond to guanosine- or uridine-rich singlestranded RNA (ssRNA) from viruses and the synthetic imidazoquinoline compounds imiquimod and R‑848.PMID: 18641647
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PMID: 18641647
TLR7 and TLR8 respond to guanosine- or uridine-rich singlestranded RNA (ssRNA) from viruses and the synthetic imidazoquinoline compounds imiquimod and R‑848.</csml:comment>
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PMID: 18641647, 11130078, 11470918
TLR9 seems to detect ssDNA molecules that contain unmethylated CpG-containing motifs, which are commonly found in the genomes of viruses and bacteria.</csml:comment>
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PMID: 18641647
TLR7 and TLR8 respond to guanosine- or uridine-rich singlestranded RNA (ssRNA) from viruses and the synthetic imidazoquinoline compounds imiquimod and R‑848.</csml:comment>
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PMID: 18641647
TLR7 and TLR8 respond to guanosine- or uridine-rich singlestranded RNA (ssRNA) from viruses and the synthetic imidazoquinoline compounds imiquimod and R‑848.</csml:comment>
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PMID: 18641647
TLR7 and TLR8 respond to guanosine- or uridine-rich singlestranded RNA (ssRNA) from viruses and the synthetic imidazoquinoline compounds imiquimod and R‑848.</csml:comment>
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PMID: 18641647
TLR7 and TLR8 respond to guanosine- or uridine-rich singlestranded RNA (ssRNA) from viruses and the synthetic imidazoquinoline compounds imiquimod and R‑848.</csml:comment>
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PMID: 18641647
TLR7 and TLR8 respond to guanosine- or uridine-rich singlestranded RNA (ssRNA) from viruses and the synthetic imidazoquinoline compounds imiquimod and R‑848.</csml:comment>
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<csml:comment type="text">





PMID: 18641647
TLR7 and TLR8 respond to guanosine- or uridine-rich singlestranded RNA (ssRNA) from viruses and the synthetic imidazoquinoline compounds imiquimod and R‑848.</csml:comment>
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PMID: 18641647, 17572678
Synthetic ODNs containing CpG dinucleotides can interact directly with the ectodomain of TLR9 and induce conformational changes40 that lead to downstream signalling activation.</csml:comment>
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PMID: 18641647, 15229469, 16675322
TLR4 signals through MyD88, TIRAP, TRIF and TRAM; and TLR2 uses both MyD88 and TIRAP.</csml:comment>
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PMID: 18641647, 15229469, 16675322
TLR4 signals through MyD88, TIRAP, TRIF and TRAM; and TLR2 uses both MyD88 and TIRAP.</csml:comment>
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<csml:comment type="text">





PMID: 18641647, 15229469, 16675322
TLR4 signals through MyD88, TIRAP, TRIF and TRAM; and TLR2 uses both MyD88 and TIRAP.</csml:comment>
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<csml:comment type="text">




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<csml:comment type="text">





PMID: 18641647, 15229469, 16675322
TLR4 signals through MyD88, TIRAP, TRIF and TRAM; and TLR2 uses both MyD88 and TIRAP.</csml:comment>
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PMID: 18641647, 15229469, 16675322
TLR4 signals through MyD88, TIRAP, TRIF and TRAM; and TLR2 uses both MyD88 and TIRAP.</csml:comment>
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PMID: 18641647, 15229469, 16675322
TLR4 signals through MyD88, TIRAP, TRIF and TRAM; and TLR2 uses both MyD88 and TIRAP.</csml:comment>
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<csml:comment type="text">




PMID: 18641647
TLR3, which is localized in endosomes, recognizes viral dsRNA and its synthetic mimic polyI:C.</csml:comment>
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<csml:comment type="text">




PMID: 18641647
TLR3, which is localized in endosomes, recognizes viral dsRNA and its synthetic mimic polyI:C.</csml:comment>
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PMID: 18641647, 12471095, 12855817
Indeed, TLR3 was shown to associate with TRIF and signal through IRF3, a key factor involved in IFNbeta production.</csml:comment>
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PMID: 18641647
Endosomal Toll-like receptor 7 (TLR7), TLR8 and TLR9 recognize RNA and DNA ligands, and signal through a key adaptor MyD88 (myeloid differentiation primary-response gene 88) in the cytosol.</csml:comment>
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PMID: 18641647
Endosomal Toll-like receptor 7 (TLR7), TLR8 and TLR9 recognize RNA and DNA ligands, and signal through a key adaptor MyD88 (myeloid differentiation primary-response gene 88) in the cytosol.</csml:comment>
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<csml:comment type="text">




PMID: 18641647
Endosomal Toll-like receptor 7 (TLR7), TLR8 and TLR9 recognize RNA and DNA ligands, and signal through a key adaptor MyD88 (myeloid differentiation primary-response gene 88) in the cytosol.</csml:comment>
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PMID: 18641647
MyD88 in turn associates with a signal complex comprised of TRAF6 (tumour-necrosis factor (TNF)-receptor-associated factor 6), BTK (Bruton’s tyrosine kinase), IRAK4 (interleukin- receptor (IL-1R)-associated kinase 4) and IRAK1, which leads to the activation of IRF7 (interferon-regulatory factor 7), NF‑kappaB (nuclear factorkappaB) and MAPKs (mitogen-activated protein kinases).</csml:comment>
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PMID: 18641647
MyD88 in turn associates with a signal complex comprised of TRAF6 (tumour-necrosis factor (TNF)-receptor-associated factor 6), BTK (Bruton’s tyrosine kinase), IRAK4 (interleukin- receptor (IL-1R)-associated kinase 4) and IRAK1, which leads to the activation of IRF7 (interferon-regulatory factor 7), NF‑kappaB (nuclear factorkappaB) and MAPKs (mitogen-activated protein kinases).</csml:comment>
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PMID: 18641647
MyD88 in turn associates with a signal complex comprised of TRAF6 (tumour-necrosis factor (TNF)-receptor-associated factor 6), BTK (Bruton’s tyrosine kinase), IRAK4 (interleukin- receptor (IL-1R)-associated kinase 4) and IRAK1, which leads to the activation of IRF7 (interferon-regulatory factor 7), NF‑kappaB (nuclear factorkappaB) and MAPKs (mitogen-activated protein kinases).</csml:comment>
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PMID: 18641647
Most importantly, IRF7 is activated through TRAF3, IRAK1, IKKalpha (inhibitor of NF-kappaB kinase alpha), osteopontin (OPN) and phosphoinositide 3-kinase (PI3K).

PMID: 18641647
MyD88 in turn associates with a signal complex comprised of TRAF6 (tumour-necrosis factor (TNF)-receptor-associated factor 6), BTK (Bruton’s tyrosine kinase), IRAK4 (interleukin- receptor (IL-1R)-associated kinase 4) and IRAK1, which leads to the activation of IRF7 (interferon-regulatory factor 7), NF‑kappaB (nuclear factorkappaB) and MAPKs (mitogen-activated protein kinases).

PMID: 18641647, 15361868
IRF7 is activated through ubiquitylation by the ubiquitin E3 ligase activity of TRAF6 (ref. 86) and phosphorylation by IRAK4.</csml:comment>
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PMID: 18641647
MyD88 in turn associates with a signal complex comprised of TRAF6 (tumour-necrosis factor (TNF)-receptor-associated factor 6), BTK (Bruton’s tyrosine kinase), IRAK4 (interleukin- receptor (IL-1R)-associated kinase 4) and IRAK1, which leads to the activation of IRF7 (interferon-regulatory factor 7), NF‑kappaB (nuclear factorkappaB) and MAPKs (mitogen-activated protein kinases).

PMID: 18641647
The MyD88–TRAF6–IRAK4 complex then activates IRF7 (interferon-regulatory factor 7), TAK1 (transforming‑growth-factor-beta-activated kinase 1), nuclear factor-kappaB (NF-kappaB) and IRF5 to propagate the downstream signals.

PMID: 18641647
TAK1 triggers the activation of NF‑kappaB and MAPKs (mitogen-activated protein kinases) and, together with IRF5, leads to the production of pro-inflammatory cytokines and the expression of co-stimulatory molecules.

PMID: 18641647
This presumably activates a different set of signal mediators, particularly NF-kappaB (nuclear factor-kappaB) and probably MAPKs (mitogen-activated protein kinases) and IRF5, and thereby leads to distinct outcomes of pDC activation without high levels of IFN production.</csml:comment>
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PMID: 18641647
MyD88 in turn associates with a signal complex comprised of TRAF6 (tumour-necrosis factor (TNF)-receptor-associated factor 6), BTK (Bruton’s tyrosine kinase), IRAK4 (interleukin- receptor (IL-1R)-associated kinase 4) and IRAK1, which leads to the activation of IRF7 (interferon-regulatory factor 7), NF‑kappaB (nuclear factorkappaB) and MAPKs (mitogen-activated protein kinases).

PMID: 18641647
TAK1 triggers the activation of NF‑kappaB and MAPKs (mitogen-activated protein kinases) and, together with IRF5, leads to the production of pro-inflammatory cytokines and the expression of co-stimulatory molecules.

PMID: 18641647
This presumably activates a different set of signal mediators, particularly NF-kappaB (nuclear factor-kappaB) and probably MAPKs (mitogen-activated protein kinases) and IRF5, and thereby leads to distinct outcomes of pDC activation without high levels of IFN production.</csml:comment>
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PMID: 18641647  
MyD88 in turn associates with a signal complex comprised of TRAF6 (tumour-necrosis factor (TNF)-receptor-associated factor 6), BTK (Bruton’s tyrosine kinase), IRAK4 (interleukin-1- receptor (IL-1R)-associated kinase 4) and IRAK1, which leads to the activation of IRF7 (interferon-regulatory factor 7), NFkappaB (nuclear factorkappaB) and MAPKs (mitogen-activated protein kinases).



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PMID: 18641647, 15361868
IRF7 is activated through ubiquitylation by the ubiquitin E3 ligase activity of TRAF6 (ref. 86) and phosphorylation by IRAK4.</csml:comment>
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PMID: 18641647  
MyD88 in turn associates with a signal complex comprised of TRAF6 (tumour-necrosis factor (TNF)-receptor-associated factor 6), BTK (Bruton’s tyrosine kinase), IRAK4 (interleukin-1- receptor (IL-1R)-associated kinase 4) and IRAK1, which leads to the activation of IRF7 (interferon-regulatory factor 7), NFkappaB (nuclear factorkappaB) and MAPKs (mitogen-activated protein kinases).



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PMID: 18641647  
MyD88 in turn associates with a signal complex comprised of TRAF6 (tumour-necrosis factor (TNF)-receptor-associated factor 6), BTK (Bruton’s tyrosine kinase), IRAK4 (interleukin-1- receptor (IL-1R)-associated kinase 4) and IRAK1, which leads to the activation of IRF7 (interferon-regulatory factor 7), NFkappaB (nuclear factorkappaB) and MAPKs (mitogen-activated protein kinases).



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PMID: 18641647
The MyD88–TRAF6–IRAK4 complex then activates IRF7 (interferon-regulatory factor 7), TAK1 (transforming‑growth-factor-beta-activated kinase 1), nuclear factor-kappaB (NF-kappaB) and IRF5 to propagate the downstream signals.


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PMID: 18641647
Most importantly, IRF7 is activated through TRAF3, IRAK1, IKKalpha (inhibitor of NF-kappaB kinase alpha), osteopontin (OPN) and phosphoinositide 3-kinase (PI3K).</csml:comment>
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PMID: 18641647
MyD88 in turn associates with a signal complex comprised of TRAF6 (tumour-necrosis factor (TNF)-receptor-associated factor 6), BTK (Bruton’s tyrosine kinase), IRAK4 (interleukin- receptor (IL-1R)-associated kinase 4) and IRAK1, which leads to the activation of IRF7 (interferon-regulatory factor 7), NF‑kappaB (nuclear factorkappaB) and MAPKs (mitogen-activated protein kinases).

PMID: 18641647
TAK1 triggers the activation of NF‑kappaB and MAPKs (mitogen-activated protein kinases) and, together with IRF5, leads to the production of pro-inflammatory cytokines and the expression of co-stimulatory molecules.

PMID: 18641647
The TLR3–TRIF signalling pathway also activates NF‑kappaB and MAPKs and results in the production of pro-inflammatory cytokines and the expression of co-stimulatory molecules (CD80 and CD86).

PMID: 18641647
Interestingly, when A-type CpG ODNs are disrupted into monomeric structures, they fail to be retained in the early endosome and to induce high amounts of type I IFN production, but instead rapidly traffic to late endosomes and induce maturation and production of IL-6 and TNF.

PMID: 18641647
This presumably activates a different set of signal mediators, particularly NF-kappaB (nuclear factor-kappaB) and probably MAPKs (mitogen-activated protein kinases) and IRF5, and thereby leads to distinct outcomes of pDC activation without high levels of IFN production.</csml:comment>
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<csml:comment type="text">Indirect</csml:comment>
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PMID: 18641647
The MyD88–TRAF6–IRAK4 complex then activates IRF7 (interferon-regulatory factor 7), TAK1 (transforming‑growth-factor-beta-activated kinase 1), nuclear factor-kappaB (NF-kappaB) and IRF5 to propagate the downstream signals.</csml:comment>
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PMID: 18641647
Following ubiquitylation and phosphorylation, IRF7 translocates to the nucleus and initiates the transcription of type I interferons (such as IFNalpha, IFNbeta, IFNlambda and IFNomega).

PMID: 18641647
Aggregated self-DNA–LL37 complexes are retained in the early endosomes of pDCs, and, similar to A-type CpG ODNs,  they trigger the TLR9–MyD88–IRF7 pathway of type I IFN production without inducing pDC maturation.</csml:comment>
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PMID: 18641647
Following ubiquitylation and phosphorylation, IRF7 translocates to the nucleus and initiates the transcription of type I interferons (such as IFNalpha, IFNbeta, IFNlambda and IFNomega).

PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.

PMID: 18641647
Aggregated self-DNA–LL37 complexes are retained in the early endosomes of pDCs, and, similar to A-type CpG ODNs,  they trigger the TLR9–MyD88–IRF7 pathway of type I IFN production without inducing pDC maturation.</csml:comment>
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PMID: 18641647
Following ubiquitylation and phosphorylation, IRF7 translocates to the nucleus and initiates the transcription of type I interferons (such as IFNalpha, IFNbeta, IFNlambda and IFNomega).

PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.

PMID: 18641647
Aggregated self-DNA–LL37 complexes are retained in the early endosomes of pDCs, and, similar to A-type CpG ODNs,  they trigger the TLR9–MyD88–IRF7 pathway of type I IFN production without inducing pDC maturation.</csml:comment>
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PMID: 18641647
Following ubiquitylation and phosphorylation, IRF7 translocates to the nucleus and initiates the transcription of type I interferons (such as IFNalpha, IFNbeta, IFNlambda and IFNomega).

PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.

PMID: 18641647
Aggregated self-DNA–LL37 complexes are retained in the early endosomes of pDCs, and, similar to A-type CpG ODNs,  they trigger the TLR9–MyD88–IRF7 pathway of type I IFN production without inducing pDC maturation.</csml:comment>
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<csml:comment type="text">




PMID: 18641647
Following ubiquitylation and phosphorylation, IRF7 translocates to the nucleus and initiates the transcription of type I interferons (such as IFNalpha, IFNbeta, IFNlambda and IFNomega).

PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.

PMID: 18641647
Aggregated self-DNA–LL37 complexes are retained in the early endosomes of pDCs, and, similar to A-type CpG ODNs,  they trigger the TLR9–MyD88–IRF7 pathway of type I IFN production without inducing pDC maturation.</csml:comment>
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PMID: 18641647
The MyD88–TRAF6–IRAK4 complex then activates IRF7 (interferon-regulatory factor 7), TAK1 (transforming‑growth-factor-beta-activated kinase 1), nuclear factor-kappaB (NF-kappaB) and IRF5 to propagate the downstream signals.</csml:comment>
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PMID: 18641647
TAK1 triggers the activation of NF‑kappaB and MAPKs (mitogen-activated protein kinases) and, together with IRF5, leads to the production of pro-inflammatory cytokines and the expression of co-stimulatory molecules.




PMID: 18641647
Interestingly, when A-type CpG ODNs are disrupted into monomeric structures, they fail to be retained in the early endosome and to induce high amounts of type I IFN production, but instead rapidly traffic to late endosomes and induce maturation and production of IL-6 and TNF.

PMID: 18641647
This presumably activates a different set of signal mediators, particularly NF-kappaB (nuclear factor-kappaB) and probably MAPKs (mitogen-activated protein kinases) and IRF5, and thereby leads to distinct outcomes of pDC activation without high levels of IFN production.</csml:comment>
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PMID: 18641647
Overall, this pathway potently induces the production of high levels of type I IFNs (such as IFNalpha, IFNbeta, IFNlambda and IFNomega), pro-inflammatory cytokines and expression of co-stimulatory molecules.

PMID: 18641647
Interestingly, when A-type CpG ODNs are disrupted into monomeric structures, they fail to be retained in the early endosome and to induce high amounts of type I IFN production, but instead rapidly traffic to late endosomes and induce maturation and production of IL-6 and TNF.

PMID: 18641647, 11160284, 11561001, 7700380
On the other hand, B-type CpG ODNs can activate B cells but only trigger pDCs to produce the pro-inflammatory cytokines TNF and IL-6, and small amounts of IFN, as well as inducing the upregulation of CD80, CD86 and the expression of MHC class II molecules.</csml:comment>
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<csml:comment type="text">




PMID: 18641647
Overall, this pathway potently induces the production of high levels of type I IFNs (such as IFNalpha, IFNbeta, IFNlambda and IFNomega), pro-inflammatory cytokines and expression of co-stimulatory molecules.

PMID: 18641647
Interestingly, when A-type CpG ODNs are disrupted into monomeric structures, they fail to be retained in the early endosome and to induce high amounts of type I IFN production, but instead rapidly traffic to late endosomes and induce maturation and production of IL-6 and TNF.

PMID: 18641647, 11160284, 11561001, 7700380
On the other hand, B-type CpG ODNs can activate B cells but only trigger pDCs to produce the pro-inflammatory cytokines TNF and IL-6, and small amounts of IFN, as well as inducing the upregulation of CD80, CD86 and the expression of MHC class II molecules.</csml:comment>
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<csml:comment type="text">




PMID: 18641647
Overall, this pathway potently induces the production of high levels of type I IFNs (such as IFNalpha, IFNbeta, IFNlambda and IFNomega), pro-inflammatory cytokines and expression of co-stimulatory molecules.

PMID: 18641647
The TLR3–TRIF signalling pathway also activates NF‑kappaB and MAPKs and results in the production of pro-inflammatory cytokines and the expression of co-stimulatory molecules (CD80 and CD86).

PMID: 18641647, 11160284, 11561001, 7700380
On the other hand, B-type CpG ODNs can activate B cells but only trigger pDCs to produce the pro-inflammatory cytokines TNF and IL-6, and small amounts of IFN, as well as inducing the upregulation of CD80, CD86 and the expression of MHC class II molecules.</csml:comment>
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PMID: 18641647
Overall, this pathway potently induces the production of high levels of type I IFNs (such as IFNalpha, IFNbeta, IFNlambda and IFNomega), pro-inflammatory cytokines and expression of co-stimulatory molecules.

PMID: 18641647
The TLR3–TRIF signalling pathway also activates NF‑kappaB and MAPKs and results in the production of pro-inflammatory cytokines and the expression of co-stimulatory molecules (CD80 and CD86).

PMID: 18641647, 11160284, 11561001, 7700380
On the other hand, B-type CpG ODNs can activate B cells but only trigger pDCs to produce the pro-inflammatory cytokines TNF and IL-6, and small amounts of IFN, as well as inducing the upregulation of CD80, CD86 and the expression of MHC class II molecules.</csml:comment>
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PMID: 18641647
Alternatively, the binding of double-stranded RNA (dsRNA) to endosomal TLR3 triggers a signalling pathway mediated by TRIF (Toll/IL-1R (TIR) domain-containing adaptor protein inducing IFNbeta), which involves TRAF3, TBK1 (TANK-binding kinase 1) and IKKepsilon (inhibitor of NF‑kappaB kinase epsilon).

PMID: 18641647
By coupling with TRAF3, TBK1 and IKKepsilon, IPS1 directly activates IRF3 and NF‑kappaB through FADD (FAS-associated via death domain), caspase‑8 and caspase‑10.</csml:comment>
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PMID: 18641647
Subsequent IRF3 activation leads to IFNbeta production.</csml:comment>
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<csml:comment type="text">



PMID: 18641647
Subsequent IRF3 activation leads to IFNbeta production.

PMID: 18641647, 17993619
Last, P2Y receptors, a family of G-protein-coupled receptors, downregulate IFNalpha secretion by human pDCs following stimulation by nucleotides such as ATP, ADP and UDP-glucose.

PMID: 18641647, 17993619
The nucleotides that bind to P2Y receptors are also known to be released and to accumulate at sites of cell stress and tissue damage.

PMID: 18641647, 16735691, 17850179
Activation of the BCR-like signalling pathway in pDCs potently suppresses the activation of both TLR7 and TLR9, inhibiting the production of all type I IFNs, as well as TNF and IL-6.</csml:comment>
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PMID: 18641647
The TLR3–TRIF signalling pathway also activates NF‑kappaB and MAPKs and results in the production of pro-inflammatory cytokines and the expression of co-stimulatory molecules (CD80 and CD86).</csml:comment>
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PMID: 18641647
The TLR3–TRIF signalling pathway also activates NF‑kappaB and MAPKs and results in the production of pro-inflammatory cytokines and the expression of co-stimulatory molecules (CD80 and CD86).</csml:comment>
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PMID: 18641647
The dsRNA receptors RIG‑I (retinoic-acid-inducible gene I), MDA5 (melanoma differentiation-associated gene 5) and LGP2 (laboratory of genetics and physiology 2) constitute the third nucleic-acid sensor system, exclusively located in the cytoplasm of most cells.</csml:comment>
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PMID: 18641647
The dsRNA receptors RIG‑I (retinoic-acid-inducible gene I), MDA5 (melanoma differentiation-associated gene 5) and LGP2 (laboratory of genetics and physiology 2) constitute the third nucleic-acid sensor system, exclusively located in the cytoplasm of most cells.</csml:comment>
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PMID: 18641647
The dsRNA receptors RIG‑I (retinoic-acid-inducible gene I), MDA5 (melanoma differentiation-associated gene 5) and LGP2 (laboratory of genetics and physiology 2) constitute the third nucleic-acid sensor system, exclusively located in the cytoplasm of most cells.</csml:comment>
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PMID: 18641647
RIGI, MDA5 and LGP2 signal through a common adaptor molecule IPS1 (IFNB-promoter stimulator 1), which is associated with the mitochondria.</csml:comment>
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PMID: 18641647
RIGI, MDA5 and LGP2 signal through a common adaptor molecule IPS1 (IFNB-promoter stimulator 1), which is associated with the mitochondria.</csml:comment>
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PMID: 18641647
RIGI, MDA5 and LGP2 signal through a common adaptor molecule IPS1 (IFNB-promoter stimulator 1), which is associated with the mitochondria.</csml:comment>
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<csml:comment type="text">



PMID: 18641647
By coupling with TRAF3, TBK1 and IKKepsilon, IPS1 directly activates IRF3 and NF‑kappaB through FADD (FAS-associated via death domain), caspase8 and caspase10.</csml:comment>
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PMID: 18641647
By coupling with TRAF3, TBK1 and IKKepsilon, IPS1 directly activates IRF3 and NF‑kappaB through FADD (FAS-associated via death domain), caspase8 and caspase10.</csml:comment>
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PMID: 18641647
By coupling with TRAF3, TBK1 and IKKepsilon, IPS1 directly activates IRF3 and NF‑kappaB through FADD (FAS-associated via death domain), caspase8 and caspase10.</csml:comment>
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PMID: 18641647
By coupling with TRAF3, TBK1 and IKKepsilon, IPS1 directly activates IRF3 and NF‑kappaB through FADD (FAS-associated via death domain), caspase8 and caspase10.</csml:comment>
</csml:comments>
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<csml:comment type="text">


PMID: 18641647, 17653195
First, a recently described molecule termed DNA-dependent activator of IRFs (DAI) has been shown in vitro to act as a cytosolic DNA sensor by binding dsDNA and signalling through TBK1 and IRF3 to activate NF-kappaB and induce type I IFN production.</csml:comment>
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PMID: 18641647, 17653195
First, a recently described molecule termed DNA-dependent activator of IRFs (DAI) has been shown in vitro to act as a cytosolic DNA sensor by binding dsDNA and signalling through TBK1 and IRF3 to activate NF-kappaB and induce type I IFN production.</csml:comment>
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PMID: 18641647, 17653195
First, a recently described molecule termed DNA-dependent activator of IRFs (DAI) has been shown in vitro to act as a cytosolic DNA sensor by binding dsDNA and signalling through TBK1 and IRF3 to activate NF-kappaB and induce type I IFN production.</csml:comment>
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PMID: 18641647, 17653195
First, a recently described molecule termed DNA-dependent activator of IRFs (DAI) has been shown in vitro to act as a cytosolic DNA sensor by binding dsDNA and signalling through TBK1 and IRF3 to activate NF-kappaB and induce type I IFN production.</csml:comment>
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<csml:comment type="text">


PMID: 18641647, 17653195
First, a recently described molecule termed DNA-dependent activator of IRFs (DAI) has been shown in vitro to act as a cytosolic DNA sensor by binding dsDNA and signalling through TBK1 and IRF3 to activate NF-kappaB and induce type I IFN production.

PMID: 18641647
This ITAM-mediated pathway potently inhibits type I interferon (IFN) and cytokine production by pDCs in response to Toll-like receptor (TLR) activation.

PMID: 18641647, 16735691, 17850179
Activation of the BCR-like signalling pathway in pDCs potently suppresses the activation of both TLR7 and TLR9, inhibiting the production of all type I IFNs, as well as TNF and IL-6.</csml:comment>
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PMID: 18641647, 18048689
For example, RNAs with short stem-loops can activate IFNinducible dsRNA-dependent protein kinase R (PKR) in a 5'-triphosphate-dependent manner, independent of RIG-I.</csml:comment>
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PMID: 18641647, 17653195
In addition, activation of the ribonuclease L by 2′,5′-linked oligoadenylate leads to the production of small RNA cleavage products from self RNA, which then function to amplify antiviral IFN responses.</csml:comment>
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PMID: 18641647, 17653195
In addition, activation of the ribonuclease L by 2′,5′-linked oligoadenylate leads to the production of small RNA cleavage products from self RNA, which then function to amplify antiviral IFN responses.</csml:comment>
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PMID: 18641647, 11790540
In most cells, the production of IFN-alpha depends on type I IFN receptor (IFNAR) triggering by IFN-beta, which results in IRF7 induction.</csml:comment>
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PMID: 18641647, 11790540
In most cells, the production of IFN-alpha depends on type I IFN receptor (IFNAR) triggering by IFN-beta, which results in IRF7 induction.</csml:comment>
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PMID: 18641647, 11790540
In most cells, the production of IFN-alpha depends on type I IFN receptor (IFNAR) triggering by IFN-beta, which results in IRF7 induction.

PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.

PMID: 18641647
This ITAM-mediated pathway potently inhibits type I interferon (IFN) and cytokine production by pDCs in response to Toll-like receptor (TLR) activation.

PMID: 18641647, 16735691, 17850179
Activation of the BCR-like signalling pathway in pDCs potently suppresses the activation of both TLR7 and TLR9, inhibiting the production of all type I IFNs, as well as TNF and IL-6.</csml:comment>
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PMID: 18641647, 17702615, 12538667
IRF8 can further amplify the IFN response during the second phase of type I IFN gene transcription in pDCs.</csml:comment>
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PMID: 18641647, 17360658, 17513736, 15665823
Aside from IRF7, IRF5 directly interacts with MyD88 and mediates the TLR-dependent induction of type I IFNs and pro-inflammatory cytokines,  including IL-6 and TNF.

PMID: 18641647, 15665823
However, IRF4 competes with IRF5, but not IRF7, to interact with MyD88, thereby negatively regulating cytokine production induced by TLR stimulation.</csml:comment>
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<csml:comment type="text">


PMID: 18641647, 17360658, 17513736, 15665823
Aside from IRF7, IRF5 directly interacts with MyD88 and mediates the TLR-dependent induction of type I IFNs and pro-inflammatory cytokines,  including IL-6 and TNF.</csml:comment>
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PMID: 18641647, 17360658, 17513736, 15665823
Aside from IRF7, IRF5 directly interacts with MyD88 and mediates the TLR-dependent induction of type I IFNs and pro-inflammatory cytokines,  including IL-6 and TNF.</csml:comment>
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PMID: 18641647, 17360658, 17513736, 15665823
Aside from IRF7, IRF5 directly interacts with MyD88 and mediates the TLR-dependent induction of type I IFNs and pro-inflammatory cytokines,  including IL-6 and TNF.</csml:comment>
</csml:comments>
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PMID: 18641647, 17360658, 17513736, 15665823
Aside from IRF7, IRF5 directly interacts with MyD88 and mediates the TLR-dependent induction of type I IFNs and pro-inflammatory cytokines,  including IL-6 and TNF.</csml:comment>
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<csml:comment type="text">


PMID: 18641647, 17360658, 17513736, 15665823
Aside from IRF7, IRF5 directly interacts with MyD88 and mediates the TLR-dependent induction of type I IFNs and pro-inflammatory cytokines,  including IL-6 and TNF.</csml:comment>
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<csml:comment type="text">


PMID: 18641647, 17360658, 17513736, 15665823
Aside from IRF7, IRF5 directly interacts with MyD88 and mediates the TLR-dependent induction of type I IFNs and pro-inflammatory cytokines,  including IL-6 and TNF.</csml:comment>
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<csml:comment type="text">


PMID: 18641647, 17360658, 17513736, 15665823
Aside from IRF7, IRF5 directly interacts with MyD88 and mediates the TLR-dependent induction of type I IFNs and pro-inflammatory cytokines,  including IL-6 and TNF.</csml:comment>
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PMID: 18641647, 17360658, 17513736, 15665823
Aside from IRF7, IRF5 directly interacts with MyD88 and mediates the TLR-dependent induction of type I IFNs and pro-inflammatory cytokines,  including IL-6 and TNF.</csml:comment>
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PMID: 18641647, 17360658, 17513736, 15665823
Aside from IRF7, IRF5 directly interacts with MyD88 and mediates the TLR-dependent induction of type I IFNs and pro-inflammatory cytokines,  including IL-6 and TNF.</csml:comment>
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PMID: 18641647, 15665823
However, IRF4 competes with IRF5, but not IRF7, to interact with MyD88, thereby negatively regulating cytokine production induced by TLR stimulation.</csml:comment>
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PMID: 18641647
Resting plasmacytoid dendritic cells (pDCs) predominantly express Toll-like receptor 7 (TLR7) and TLR9, which reside in the endoplasmic reticulum (ER) in association with UNC93B and gp96.

PMID: 18641647, 16415873, 17452530
The delivery of TLRs to endolysosomes and their subsequent proper activation requires UNC93B, an ER-resident transmembrane protein that can specifically interact with TLR3, TLR7 and TLR9.</csml:comment>
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PMID: 18641647
Resting plasmacytoid dendritic cells (pDCs) predominantly express Toll-like receptor 7 (TLR7) and TLR9, which reside in the endoplasmic reticulum (ER) in association with UNC93B and gp96.

PMID: 18641647, 16415873, 17452530
The delivery of TLRs to endolysosomes and their subsequent proper activation requires UNC93B, an ER-resident transmembrane protein that can specifically interact with TLR3, TLR7 and TLR9.</csml:comment>
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PMID: 18641647
Resting plasmacytoid dendritic cells (pDCs) predominantly express Toll-like receptor 7 (TLR7) and TLR9, which reside in the endoplasmic reticulum (ER) in association with UNC93B and gp96.

PMID: 18641647, 16415873, 17452530
The delivery of TLRs to endolysosomes and their subsequent proper activation requires UNC93B, an ER-resident transmembrane protein that can specifically interact with TLR3, TLR7 and TLR9.</csml:comment>
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PMID: 18641647, 11160284, 11561001, 7700380
On the other hand, B-type CpG ODNs can activate B cells but only trigger pDCs to produce the pro-inflammatory cytokines TNF and IL-6, and small amounts of IFN, as well as inducing the upregulation of CD80, CD86 and the expression of MHC class II molecules.</csml:comment>
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PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.</csml:comment>
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PMID: 18641647, 16415873   
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.
</csml:comment>
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PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.

PMID: 18641647
Aggregated self-DNA–LL37 complexes are retained in the early endosomes of pDCs, and, similar to A-type CpG ODNs,  they trigger the TLR9–MyD88–IRF7 pathway of type I IFN production without inducing pDC maturation.</csml:comment>
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PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.

PMID: 18641647
Aggregated self-DNA–LL37 complexes are retained in the early endosomes of pDCs, and, similar to A-type CpG ODNs,  they trigger the TLR9–MyD88–IRF7 pathway of type I IFN production without inducing pDC maturation.</csml:comment>
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PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.

PMID: 18641647
This ITAM-mediated pathway potently inhibits type I interferon (IFN) and cytokine production by pDCs in response to Toll-like receptor (TLR) activation.

PMID: 18641647, 16735691, 17850179
Activation of the BCR-like signalling pathway in pDCs potently suppresses the activation of both TLR7 and TLR9, inhibiting the production of all type I IFNs, as well as TNF and IL-6.</csml:comment>
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PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.

PMID: 18641647, 16735691, 17850179
Activation of the BCR-like signalling pathway in pDCs potently suppresses the activation of both TLR7 and TLR9, inhibiting the production of all type I IFNs, as well as TNF and IL‑6.</csml:comment>
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PMID: 18641647, 16415873
The prolonged  retention of multimeric A-type CpG ODNs provides a platform for extended activation of the signal-transducing complex, consisting of MyD88 and IRF7, which leads to robust type I IFN production.

PMID: 18641647
This ITAM-mediated pathway potently inhibits type I interferon (IFN) and cytokine production by pDCs in response to Toll-like receptor (TLR) activation.

PMID: 18641647, 16735691, 17850179
Activation of the BCR-like signalling pathway in pDCs potently suppresses the activation of both TLR7 and TLR9, inhibiting the production of all type I IFNs, as well as TNF and IL-6.</csml:comment>
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PMID: 18641647, 15591070, 15815647, 16864658
Conversely, liposome or particle encapsidation of B-type CpG ODNs allows their retention in early endosomes and the subsequent induction of much higher levels of type I IFNs and lower levels of IL-6 and TNF and impaired pDC maturation, which supports the important link between the physical size of TLR9 ligands and their stimulatory capacity.
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PMID: 18641647
This presumably activates a different set of signal mediators, particularly NF-kappaB (nuclear factor-kappaB) and probably MAPKs (mitogen-activated protein kinases) and IRF5, and thereby leads to distinct outcomes of pDC activation without high levels of IFN production.</csml:comment>
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PMID: 18641647
Interestingly, when A-type CpG ODNs are disrupted into monomeric structures, they fail to be retained in the early endosome and to induce high amounts of type I IFN production, but instead rapidly traffic to late endosomes and induce maturation and production of IL-6 and TNF.

PMID: 18641647
This ITAM-mediated pathway potently inhibits type I interferon (IFN) and cytokine production by pDCs in response to Toll-like receptor (TLR) activation.

PMID: 18641647, 16735691, 17850179
Activation of the BCR-like signalling pathway in pDCs potently suppresses the activation of both TLR7 and TLR9, inhibiting the production of all type I IFNs, as well as TNF and IL-6.</csml:comment>
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PMID: 18641647
Interestingly, when A-type CpG ODNs are disrupted into monomeric structures, they fail to be retained in the early endosome and to induce high amounts of type I IFN production, but instead rapidly traffic to late endosomes and induce maturation and production of IL-6 and TNF.

PMID: 18641647
This ITAM-mediated pathway potently inhibits type I interferon (IFN) and cytokine production by pDCs in response to Toll-like receptor (TLR) activation.

PMID: 18641647, 16735691, 17850179
Activation of the BCR-like signalling pathway in pDCs potently suppresses the activation of both TLR7 and TLR9, inhibiting the production of all type I IFNs, as well as TNF and IL-6.</csml:comment>
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PMID: 18641647, 15591070, 15815647, 16864658
Conversely, liposome or particle encapsidation of B-type CpG ODNs allows their retention in early endosomes and the subsequent induction of much higher levels of type I IFNs and lower levels of IL-6 and TNF and impaired pDC maturation, which supports the important link between the physical size of TLR9 ligands and their stimulatory capacity.</csml:comment>
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PMID: 18641647
Interestingly, when A-type CpG ODNs are disrupted into monomeric structures, they fail to be retained in the early endosome and to induce high amounts of type I IFN production, but instead rapidly traffic to late endosomes and induce maturation and production of IL-6 and TNF.</csml:comment>
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PMID: 18641647
This presumably activates a different set of signal mediators, particularly NF-kappaB (nuclear factor-kappaB) and probably MAPKs (mitogen-activated protein kinases) and IRF5, and thereby leads to distinct outcomes of pDC activation without high levels of IFN production.</csml:comment>
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PMID: 18641647
The antimicrobial peptide LL37 is secreted by damaged epithelial cells or deposited by tissue-infiltrating neutrophils. It binds self-DNA fragments released by dying cells to form aggregated and condensed structures that are protected from extracellular nuclease degradation and delivered via lipid rafts from the extracellular environment into the early endosomes of plasmacytoid dendritic cells (pDCs).</csml:comment>
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PMID: 18641647
Dying cells also release high-mobility group box 1 protein (HMGB1), which binds aggregated self-DNA–LL37 complexes and promotes their association with Toll-like receptor 9 (TLR9) in early endosomes by binding to RAGE (receptor for advanced glycation  end-products).

PMID: 18641647
Interestingly, in contrast to LL37, HMGB1 can only bind multimeric aggregated DNA structures, such as A-type CpG ODNs, and not monomeric DNA sequences, such as B-type CpG ODNs.</csml:comment>
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PMID: 18641647
Dying cells also release high-mobility group box 1 protein (HMGB1), which binds aggregated self-DNA–LL37 complexes and promotes their association with Toll-like receptor 9 (TLR9) in early endosomes by binding to RAGE (receptor for advanced glycation  end-products).</csml:comment>
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PMID: 18641647
Dying cells also release high-mobility group box 1 protein (HMGB1), which binds aggregated self-DNA–LL37 complexes and promotes their association with Toll-like receptor 9 (TLR9) in early endosomes by binding to RAGE (receptor for advanced glycation  end-products).</csml:comment>
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PMID: 18641647
Aggregated self-DNA–LL37 complexes are retained in the early endosomes of pDCs, and, similar to A-type CpG ODNs,  they trigger the TLR9–MyD88–IRF7 pathway of type I IFN production without inducing pDC maturation.</csml:comment>
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PMID: 18641647
Aggregated self-DNA–LL37 complexes are retained in the early endosomes of pDCs, and, similar to A-type CpG ODNs,  they trigger the TLR9–MyD88–IRF7 pathway of type I IFN production without inducing pDC maturation.</csml:comment>
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PMID: 18641647
After internalization, the self-DNA–LL37–HMGB1 complex associates with TLR9 in early endosomes by engaging RAGE.</csml:comment>
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PMID: 18641647
DNA-specific IgG antibodies can bind self-DNA–LL37–HMGB1 complexes and potently enhance the internalization of the complex through FcgammaRIIA.</csml:comment>
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PMID: 18641647
DNA-specific IgG antibodies can bind self-DNA–LL37–HMGB1 complexes and potently enhance the internalization of the complex through FcgammaRIIA.</csml:comment>
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PMID: 18641647, 11711679
The ongoing production of type I IFNs by pDCs in these patients induces an unabated activation and maturation of mDCs that stimulate autoreactive T cells.</csml:comment>
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PMID: 18641647, 12932356
Furthermore, pDC-derived type I IFNs, together with IL-6, stimulate the differentiation of autoreactive B cells into autoantibody-secreting plasma cells.</csml:comment>
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PMID: 18641647, 16330816
However, self-RNA molecules, in particular those rich in uridine or uridine and guanosine (U/UGRNA) and those in small nuclear ribonucleoprotein (snRNP), were shown to trigger pDCs to produce type I IFNs through TLR7 when delivered to endosomes by autoantibodies or liposomes.</csml:comment>
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PMID: 18641647, 16330816
However, self-RNA molecules, in particular those rich in uridine or uridine and guanosine (U/UGRNA) and those in small nuclear ribonucleoprotein (snRNP), were shown to trigger pDCs to produce type I IFNs through TLR7 when delivered to endosomes by autoantibodies or liposomes.

PMID: 18641647
This ITAM-mediated pathway potently inhibits type I interferon (IFN) and cytokine production by pDCs in response to Toll-like receptor (TLR) activation.

PMID: 18641647, 16735691, 17850179
Activation of the BCR-like signalling pathway in pDCs potently suppresses the activation of both TLR7 and TLR9, inhibiting the production of all type I IFNs, as well as TNF and IL‑6.</csml:comment>
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Both BDCA2 and ILT7 associate with the γ‑chain of the highaffinity Fc receptor for IgE (FcepsilonRIgamma) and activate pDCs through an immunoreceptor-based tyrosine activation motif  (ITAM)-mediated signalling pathway.</csml:comment>
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Both BDCA2 and ILT7 associate with the γ‑chain of the highaffinity Fc receptor for IgE (FcepsilonRIgamma) and activate pDCs through an immunoreceptor-based tyrosine activation motif  (ITAM)-mediated signalling pathway.</csml:comment>
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Crosslinking of NKp44, a receptor that signals through the ITAM-bearing adaptor DAP12,  inhibits IFNalpha production induced by CpG ODNs.
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In mice, antibody crosslinking of Siglec-H (sialicacid-binding immunoglobulin-like lectin H), another DAP12-associated receptor expressed by pDCs, reduces type I IFN production by pDCs in vitro and in vivo.</csml:comment>
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These receptor complexes or receptors with intrinsic ITAMs, such as FcgammaRIIA, signal through their ITAMs and activate a B-cell receptor (BCR)-like pathway that involves SRC family protein tyrosine kinases (PTKs), SYK (spleen tyrosine kinase) and the B-cell-specific adaptors BLNK (B-cell linker) and BCAP (B-cell adaptor protein).</csml:comment>
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<csml:comment type="text">PMID: 18641647
These receptor complexes or receptors with intrinsic ITAMs, such as FcgammaRIIA, signal through their ITAMs and activate a B-cell receptor (BCR)-like pathway that involves SRC family protein tyrosine kinases (PTKs), SYK (spleen tyrosine kinase) and the B-cell-specific adaptors BLNK (B-cell linker) and BCAP (B-cell adaptor protein).</csml:comment>
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<csml:comment type="text">PMID: 18641647
These receptor complexes or receptors with intrinsic ITAMs, such as FcgammaRIIA, signal through their ITAMs and activate a B-cell receptor (BCR)-like pathway that involves SRC family protein tyrosine kinases (PTKs), SYK (spleen tyrosine kinase) and the B-cell-specific adaptors BLNK (B-cell linker) and BCAP (B-cell adaptor protein).</csml:comment>
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<csml:comment type="text">PMID: 18641647
These receptor complexes or receptors with intrinsic ITAMs, such as FcgammaRIIA, signal through their ITAMs and activate a B-cell receptor (BCR)-like pathway that involves SRC family protein tyrosine kinases (PTKs), SYK (spleen tyrosine kinase) and the B-cell-specific adaptors BLNK (B-cell linker) and BCAP (B-cell adaptor protein).</csml:comment>
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These receptor complexes or receptors with intrinsic ITAMs, such as FcgammaRIIA, signal through their ITAMs and activate a B-cell receptor (BCR)-like pathway that involves SRC family protein tyrosine kinases (PTKs), SYK (spleen tyrosine kinase) and the B-cell-specific adaptors BLNK (B-cell linker) and BCAP (B-cell adaptor protein).</csml:comment>
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These receptor complexes or receptors with intrinsic ITAMs, such as FcgammaRIIA, signal through their ITAMs and activate a B-cell receptor (BCR)-like pathway that involves SRC family protein tyrosine kinases (PTKs), SYK (spleen tyrosine kinase) and the B-cell-specific adaptors BLNK (B-cell linker) and BCAP (B-cell adaptor protein).</csml:comment>
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These receptor complexes or receptors with intrinsic ITAMs, such as FcgammaRIIA, signal through their ITAMs and activate a B-cell receptor (BCR)-like pathway that involves SRC family protein tyrosine kinases (PTKs), SYK (spleen tyrosine kinase) and the B-cell-specific adaptors BLNK (B-cell linker) and BCAP (B-cell adaptor protein).</csml:comment>
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However, PDC-TREM (triggering receptor expressed on myeloid cells), a newly discovered pDC-specific transmembrane receptor that forms a complex with plexin A1, is activated by its endogenous ligand semaphorin  6D to induce DAP12-mediated activation of PI3K and extracellular-signal-regulated kinase 1 (ERK1) and ERK2, which leads to enhanced levels of type I IFN  production.</csml:comment>
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However, PDC-TREM (triggering receptor expressed on myeloid cells), a newly discovered pDC-specific transmembrane receptor that forms a complex with plexin A1, is activated by its endogenous ligand semaphorin  6D to induce DAP12-mediated activation of PI3K and extracellular-signal-regulated kinase 1 (ERK1) and ERK2, which leads to enhanced levels of type I IFN  production.</csml:comment>
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However, PDC-TREM (triggering receptor expressed on myeloid cells), a newly discovered pDC-specific transmembrane receptor that forms a complex with plexin A1, is activated by its endogenous ligand semaphorin  6D to induce DAP12-mediated activation of PI3K and extracellular-signal-regulated kinase 1 (ERK1) and ERK2, which leads to enhanced levels of type I IFN  production.</csml:comment>
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However, PDC-TREM (triggering receptor expressed on myeloid cells), a newly discovered pDC-specific transmembrane receptor that forms a complex with plexin A1, is activated by its endogenous ligand semaphorin  6D to induce DAP12-mediated activation of PI3K and extracellular-signal-regulated kinase 1 (ERK1) and ERK2, which leads to enhanced levels of type I IFN  production.</csml:comment>
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However, PDC-TREM (triggering receptor expressed on myeloid cells), a newly discovered pDC-specific transmembrane receptor that forms a complex with plexin A1, is activated by its endogenous ligand semaphorin  6D to induce DAP12-mediated activation of PI3K and extracellular-signal-regulated kinase 1 (ERK1) and ERK2, which leads to enhanced levels of type I IFN  production.</csml:comment>
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The nucleotides that bind to P2Y receptors are also known to be released and to accumulate at sites of cell stress and tissue damage.</csml:comment>
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These self-RNA and  autoantibody complexes were also shown to activate autoreactive B cells through the B-cell receptor (BCR) and endosomal TLR7.</csml:comment>
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These self-RNA and  autoantibody complexes were also shown to activate autoreactive B cells through the B-cell receptor (BCR) and endosomal TLR7.</csml:comment>
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By contrast, myeloid DCs (mDCs) produced type I IFNs and interleukin‑12 (IL-12) in response to polyI:C but not to CpG-containing DNA.</csml:comment>
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Interestingly, at the same time, Klinman and colleagues classified CpG ODNs into two main groups: D-type (now known as A-type) CpG ODNs, which stimulate IFNgamma production by natural killer (NK) cells, and K-type (now known as B-type) CpG ODNs, which stimulate B-cell proliferation and B-cell IL-6 and antibody production.</csml:comment>
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Interestingly, at the same time, Klinman and colleagues classified CpG ODNs into two main groups: D-type (now known as A-type) CpG ODNs, which stimulate IFNgamma production by natural killer (NK) cells, and K-type (now known as B-type) CpG ODNs, which stimulate B-cell proliferation and B-cell IL-6 and antibody production.</csml:comment>
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