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PMID: 17959357
Anti-viral responses are mediated by TLR4 which senses F protein from RSV, TLR3 which senses double-stranded RNA (poly I:C), TLR7 and TLR8 which sense single-stranded RNA (ss RNA).

PMID: 17959357
Moreover, ds-RNA released from necrotic cells and heat shock proteins expressed in the synovial tissue are able to activate TLR-3 and TLR-4, respectively.</csml:comment>
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PMID: 17959357
TLRs are able to recognize a variety of pathogen-derived products: lipopolysaccharide (LPS) is the ligand for TLR4; bacterial lipoproteins (e.g. lipotechoic acid) are recognized by a TLR2/6 dimer; triacylated lipopeptides by a TLR2/1 dimer; CpG oligonucleotides by TLR9; flagellin by TLR5.</csml:comment>
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PMID: 17959357
TLRs are able to recognize a variety of pathogen-derived products: lipopolysaccharide (LPS) is the ligand for TLR4; bacterial lipoproteins (e.g. lipotechoic acid) are recognized by a TLR2/6 dimer; triacylated lipopeptides by a TLR2/1 dimer; CpG oligonucleotides by TLR9; flagellin by TLR5.</csml:comment>
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PMID: 17959357
TLRs are able to recognize a variety of pathogen-derived products: lipopolysaccharide (LPS) is the ligand for TLR4; bacterial lipoproteins (e.g. lipotechoic acid) are recognized by a TLR2/6 dimer; triacylated lipopeptides by a TLR2/1 dimer; CpG oligonucleotides by TLR9; flagellin by TLR5.</csml:comment>
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PMID: 17959357
TLRs are able to recognize a variety of pathogen-derived products: lipopolysaccharide (LPS) is the ligand for TLR4; bacterial lipoproteins (e.g. lipotechoic acid) are recognized by a TLR2/6 dimer; triacylated lipopeptides by a TLR2/1 dimer; CpG oligonucleotides by TLR9; flagellin by TLR5.</csml:comment>
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PMID: 17959357
TLRs are able to recognize a variety of pathogen-derived products.</csml:comment>
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PMID: 17959357
TLRs are able to recognize a variety of pathogen-derived products: lipopolysaccharide (LPS) is the ligand for TLR4; bacterial lipoproteins (e.g. lipotechoic acid) are recognized by a TLR2/6 dimer; triacylated lipopeptides by a TLR2/1 dimer; CpG oligonucleotides by TLR9; flagellin by TLR5.</csml:comment>
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PMID: 17959357
A TLR2/6 dimer recognizes zymosan for anti-fungal responses.</csml:comment>
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PMID: 17959357
Anti-viral responses are mediated by TLR4 which senses F protein from RSV, TLR3 which senses double-stranded RNA (poly I:C), TLR7 and TLR8 which sense single-stranded RNA (ss RNA).</csml:comment>
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</csml:comment>
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PMID: 17959357
Products of inflamed tissue (e.g. hsp60, fibrinogen products) are sensed by TLR4.

PMID: 17959357, 15690042
More specifically, TLR-2 and TLR-4 can be fibrinogen, hyalouronate, heat shock proteins and modified low density lipoprotein, implying a role for their activation in the production of proinflammatory cytokines in the synovial fluid of rheumatoid arthritis patients' or the sterile inflammation of atherosclerosis.

PMID: 17959357
Moreover, ds-RNA released from necrotic cells and heat shock proteins expressed in the synovial tissue are able to activate TLR-3 and TLR-4, respectively.</csml:comment>
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PMID: 17959357
Anti-viral responses are mediated by TLR4 which senses F protein from RSV, TLR3 which senses double-stranded RNA (poly I:C), TLR7 and TLR8 which sense single-stranded RNA (ss RNA).</csml:comment>
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PMID: 17959357
Anti-viral responses are mediated by TLR4 which senses F protein from RSV, TLR3 which senses double-stranded RNA (poly I:C), TLR7 and TLR8 which sense single-stranded RNA (ss RNA).</csml:comment>
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PMID: 17959357
Products of inflamed tissue (e.g. hsp60, fibrinogen products) are sensed by TLR4.

PMID: 17959357, 15690042
More specifically, TLR-2 and TLR-4 can be fibrinogen, hyalouronate, heat shock proteins and modified low density lipoprotein, implying a role for their activation in the production of proinflammatory cytokines in the synovial fluid of rheumatoid arthritis patients' or the sterile inflammation of atherosclerosis.</csml:comment>
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Indirect</csml:comment>
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</csml:comment>
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PMID: 17959357, 15928677
Ubiquitination inducing molecules (such as TRIAD 3) that promote TLR degradation; anti-inflammatory molecules (TGF-beta) that directly down-regulate TLR expression; and TLR-induced apoptosis that prevents an excessive inflammatory reaction.</csml:comment>
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PMID: 17959357, 15928677
Ubiquitination inducing molecules (such as TRIAD 3) that promote TLR degradation; anti-inflammatory molecules (TGF-beta) that directly down-regulate TLR expression; and TLR-induced apoptosis that prevents an excessive inflammatory reaction.</csml:comment>
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PMID: 17959357, 15928677
Ubiquitination inducing molecules (such as TRIAD 3) that promote TLR degradation; anti-inflammatory molecules (TGF-beta) that directly down-regulate TLR expression; and TLR-induced apoptosis that prevents an excessive inflammatory reaction.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.

PMID: 17959357, 15814732
Recognition of the urate crystals by TLR-2 and TLR-4 results in release of nitric oxide by chondrocytes, activation of the NF-kappaB transcription factor and thus, expression of several pro-inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.</csml:comment>
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PMID: 17959357
MyD88 is the adaptor molecule, used by all but TLR-3 TLRs, which interacts with IRAK4 (IL-1 receptor associated kinase 4) and then with TRAF6 (TNF receptor-associated factor 6), resulting in activation of NF-kappaB and MAP kinases (mitogen-activated protein kinases) and transcription of inflammatory cytokines.

PMID: 17959357, 15814732
Recognition of the urate crystals by TLR-2 and TLR-4 results in release of nitric oxide by chondrocytes, activation of the NF-kappaB transcription factor and thus, expression of several pro-inflammatory cytokines.</csml:comment>
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PMID: 17959357
TRAF6 may also interact with TBK1 (TRAF-family member-associated NF-kappaB activator-binding kinase 2) to activate IRF7 (IFN regulatory factor 7) and result in IFN-alpha induction. This pathway is mediated by TLR-7, TLR-8, TLR-9.</csml:comment>
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PMID: 17959357
TRAF6 may also interact with TBK1 (TRAF-family member-associated NF-kappaB activator-binding kinase 2) to activate IRF7 (IFN regulatory factor 7) and result in IFN-alpha induction. This pathway is mediated by TLR-7, TLR-8, TLR-9.</csml:comment>
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PMID: 17959357
TRAF6 may also interact with TBK1 (TRAF-family member-associated NF-kappaB activator-binding kinase 2) to activate IRF7 (IFN regulatory factor 7) and result in IFN-alpha induction. This pathway is mediated by TLR-7, TLR-8, TLR-9.</csml:comment>
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Indirect</csml:comment>
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PMID: 17959357
TRAF6 may also interact with TBK1 (TRAF-family member-associated NF-kappaB activator-binding kinase 2) to activate IRF7 (IFN regulatory factor 7) and result in IFN-alpha induction. This pathway is mediated by TLR-7, TLR-8, TLR-9.</csml:comment>
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PMID: 17959357
TRAF6 may also interact with TBK1 (TRAF-family member-associated NF-kappaB activator-binding kinase 2) to activate IRF7 (IFN regulatory factor 7) and result in IFN-alpha induction. This pathway is mediated by TLR-7, TLR-8, TLR-9.</csml:comment>
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PMID: 17959357
TRAF6 may also interact with TBK1 (TRAF-family member-associated NF-kappaB activator-binding kinase 2) to activate IRF7 (IFN regulatory factor 7) and result in IFN-alpha induction. This pathway is mediated by TLR-7, TLR-8, TLR-9.</csml:comment>
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PMID: 17959357
TRAF6 may also interact with TBK1 (TRAF-family member-associated NF-kappaB activator-binding kinase 2) to activate IRF7 (IFN regulatory factor 7) and result in IFN-alpha induction. This pathway is mediated by TLR-7, TLR-8, TLR-9.</csml:comment>
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PMID: 17959357
TRAF6 may also interact with TBK1 (TRAF-family member-associated NF-kappaB activator-binding kinase 2) to activate IRF7 (IFN regulatory factor 7) and result in IFN-alpha induction. This pathway is mediated by TLR-7, TLR-8, TLR-9.</csml:comment>
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PMID: 17959357
TLR-3 signals through TRIF (Toll/IL-1 receptor domain containing adaptor protein inducing IFN-beta) that activates TBK1 and IRF3 to induce IFN-beta transcription.</csml:comment>
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PMID: 17959357
TLR-3 signals through TRIF (Toll/IL-1 receptor domain containing adaptor protein inducing IFN-beta) that activates TBK1 and IRF3 to induce IFN-beta transcription.</csml:comment>
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PMID: 17959357
TLR-3 signals through TRIF (Toll/IL-1 receptor domain containing adaptor protein inducing IFN-beta) that activates TBK1 and IRF3 to induce IFN-beta transcription.

PMID: 17959357
In the TLR4- and TLR3-mediated signaling pathways, IRF3 is activated via TBK1 and IKKepsilon/IKK-i (MyD88-independent pathway).</csml:comment>
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PMID: 17959357
TRAF6 may also interact with TBK1 (TRAF-family member-associated NF-kappaB activator-binding kinase 2) to activate IRF7 (IFN regulatory factor 7) and result in IFN-alpha induction. This pathway is mediated by TLR-7, TLR-8, TLR-9.</csml:comment>
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Indirect</csml:comment>
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PMID: 17959357
TRAF6 may also interact with TBK1 (TRAF-family member-associated NF-kappaB activator-binding kinase 2) to activate IRF7 (IFN regulatory factor 7) and result in IFN-alpha induction. This pathway is mediated by TLR-7, TLR-8, TLR-9.</csml:comment>
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PMID: 17959357
TLR-3 signals through TRIF (Toll/IL-1 receptor domain containing adaptor protein inducing IFN-beta) that activates TBK1 and IRF3 to induce IFN-beta transcription.</csml:comment>
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PMID: 17959357
TLR-3 signals through TRIF (Toll/IL-1 receptor domain containing adaptor protein inducing IFN-beta) that activates TBK1 and IRF3 to induce IFN-beta transcription.</csml:comment>
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PMID: 17959357
Protozoal glycosyl-phosphatidyl-inositol (GPI-)anchor proteins are recognized by TLR2.</csml:comment>
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PMID: 17959357
Patients with X-linked agammaglobulinemia exhibit an impaired TLR-8-mediated IL-6 and TNF-alpha production, which may account for their increased susceptibility to enteroviral infections.</csml:comment>
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PMID: 17959357
Patients with X-linked agammaglobulinemia exhibit an impaired TLR-8-mediated IL-6 and TNF-alpha production, which may account for their increased susceptibility to enteroviral infections.</csml:comment>
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PMID: 17959357
Patients with X-linked agammaglobulinemia exhibit an impaired TLR-8-mediated IL-6 and TNF-alpha production, which may account for their increased susceptibility to enteroviral infections.</csml:comment>
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PMID: 17959357
Patients with X-linked agammaglobulinemia exhibit an impaired TLR-8-mediated IL-6 and TNF-alpha production, which may account for their increased susceptibility to enteroviral infections.</csml:comment>
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PMID: 17959357
TIR domain-containing adaptor protein (TIRAP)/MyD88-adaptor-like specifically mediates the MyD88-dependent pathway of TLR2 and TLR4.</csml:comment>
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PMID: 17959357
TIR domain-containing adaptor protein (TIRAP)/MyD88-adaptor-like specifically mediates the MyD88-dependent pathway of TLR2 and TLR4.</csml:comment>
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PMID: 17959357
TIR domain-containing adaptor protein (TIRAP)/MyD88-adaptor-like specifically mediates the MyD88-dependent pathway of TLR2 and TLR4.</csml:comment>
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PMID: 17959357
TIR domain-containing adaptor protein (TIRAP)/MyD88-adaptor-like specifically mediates the MyD88-dependent pathway of TLR2 and TLR4.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
In the TLR4- and TLR3-mediated signaling pathways, IRF3 is activated via TKB1 and IKKepsilon/IKK-i (MyD88-independent pathway).</csml:comment>
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PMID: 17959357
In the TLR4- and TLR3-mediated signaling pathways, IRF3 is activated via TKB1 and IKKepsilon/IKK-i (MyD88-independent pathway).</csml:comment>
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PMID: 17959357
In the TLR4- and TLR3-mediated signaling pathways, IRF3 is activated via TKB1 and IKKepsilon/IKK-i (MyD88-independent pathway).</csml:comment>
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PMID: 17959357
In the TLR4- and TLR3-mediated signaling pathways, IRF3 is activated via TBK1 and IKKepsilon/IKK-i (MyD88-independent pathway).</csml:comment>
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PMID: 17959357
Importantly, TLR-3, TLR-7 and TLR-8 recognize endogenous single stranded RNA.</csml:comment>
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PMID: 17959357
Importantly, TLR-3, TLR-7 and TLR-8 recognize endogenous single stranded RNA.</csml:comment>
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PMID: 17959357, 16492804
Finally, TLR-9 can be stimulated by endogenous hypomethylated DNA; the activation of TLR-9/MyD88 pathway is a prerequisite for switching to pathogenic autoantibody production in a murine model of SLE.</csml:comment>
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PMID: 17959357
The protective effect of TLR-9 may appear at first glance to be paradoxical since it has been well established that the recognition of endogenous nucleic acids by TLR-9 within the endosomal compartment induces B cell proliferation, plasmablast differentiation and, ultimately, production of pathogenic autoantibodies.</csml:comment>
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PMID: 17959357
The protective effect of TLR-9 may appear at first glance to be paradoxical since it has been well established that the recognition of endogenous nucleic acids by TLR-9 within the endosomal compartment induces B cell proliferation, plasmablast differentiation and, ultimately, production of pathogenic autoantibodies.</csml:comment>
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PMID: 17959357
The protective effect of TLR-9 may appear at first glance to be paradoxical since it has been well established that the recognition of endogenous nucleic acids by TLR-9 within the endosomal compartment induces B cell proliferation, plasmablast differentiation and, ultimately, production of pathogenic autoantibodies.</csml:comment>
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PMID: 17959357
Hydroxychloroquine, an established treatment for various aspects of lupus and an inhibitor of TLR-9 expression, also inhibited the lupus serum-mediated induction of TLR-9 on plasma cells.</csml:comment>
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PMID: 17959357, 17075805
An enhanced induction of HLA-DR was documented on TLR-9 stimulated (by means of its ligand ODN 2006) B-cells in active but not inactive SLE patients.</csml:comment>
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PMID: 17959357, 17075805
An enhanced induction of HLA-DR was documented on TLR-9 stimulated (by means of its ligand ODN 2006) B-cells in active but not inactive SLE patients.</csml:comment>
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PMID: 17959357
Importantly, TLR-3, TLR-7 and TLR-8 recognize endogenous single stranded RNA.</csml:comment>
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PMID: 17959357, 15690042
More specifically, TLR-2 and TLR-4 can be fibrinogen, hyalouronate, heat shock proteins and modified low density lipoprotein, implying a role for their activation in the production of proinflammatory cytokines in the synovial fluid of rheumatoid arthritis patients' or the sterile inflammation of atherosclerosis.</csml:comment>
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PMID: 17959357, 15690042
More specifically, TLR-2 and TLR-4 can be fibrinogen, hyalouronate, heat shock proteins and modified low density lipoprotein, implying a role for their activation in the production of proinflammatory cytokines in the synovial fluid of rheumatoid arthritis patients' or the sterile inflammation of atherosclerosis.</csml:comment>
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PMID: 17959357, 15690042
More specifically, TLR-2 and TLR-4 can be fibrinogen, hyalouronate, heat shock proteins and modified low density lipoprotein, implying a role for their activation in the production of proinflammatory cytokines in the synovial fluid of rheumatoid arthritis patients' or the sterile inflammation of atherosclerosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357, 15690042
More specifically, TLR-2 and TLR-4 can be fibrinogen, hyalouronate, heat shock proteins and modified low density lipoprotein, implying a role for their activation in the production of proinflammatory cytokines in the synovial fluid of rheumatoid arthritis patients' or the sterile inflammation of atherosclerosis.
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PMID: 17959357, 15690042
More specifically, TLR-2 and TLR-4 can be fibrinogen, hyalouronate, heat shock proteins and modified low density lipoprotein, implying a role for their activation in the production of proinflammatory cytokines in the synovial fluid of rheumatoid arthritis patients' or the sterile inflammation of atherosclerosis.</csml:comment>
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PMID: 17959357, 15690042
More specifically, TLR-2 and TLR-4 can be fibrinogen, hyalouronate, heat shock proteins and modified low density lipoprotein, implying a role for their activation in the production of proinflammatory cytokines in the synovial fluid of rheumatoid arthritis patients' or the sterile inflammation of atherosclerosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357
The matrix turn-over products generated during the acute tissue injury, provide resident or immune renal cells with abundant endogenous TLR ligands (fibrinogen, hyalouran, fibronectin, HSPs) that may induce the production of reactive oxygen species and of TGF-beta, resulting in collagen production and irreversible renal fibrosis.</csml:comment>
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PMID: 17959357, 12632416
TLR-2 activation of synovial fibroblasts through bacterial peptidoglycans results in upregulation of integrins, matrix metalloproteinases, and inflammatory cytokines (IL-6, IL-8).</csml:comment>
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PMID: 17959357, 12632416
TLR-2 activation of synovial fibroblasts through bacterial peptidoglycans results in upregulation of integrins, matrix metalloproteinases, and inflammatory cytokines (IL-6, IL-8).</csml:comment>
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PMID: 17959357, 12632416
TLR-2 activation of synovial fibroblasts through bacterial peptidoglycans results in upregulation of integrins, matrix metalloproteinases, and inflammatory cytokines (IL-6, IL-8).</csml:comment>
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PMID: 17959357, 15814732
Recognition of the urate crystals by TLR-2 and TLR-4 results in release of nitric oxide by chondrocytes, activation of the NF-kappaB transcription factor and thus, expression of several pro-inflammatory cytokines.</csml:comment>
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PMID: 17959357, 15814732
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PMID: 17959357, 15814732
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PMID: 17959357, 15814732
Recognition of the urate crystals by TLR-2 and TLR-4 results in release of nitric oxide by chondrocytes, activation of the NF-kappaB transcription factor and thus, expression of several pro-inflammatory cytokines.</csml:comment>
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PMID: 17959357, 15814732
Recognition of the urate crystals by TLR-2 and TLR-4 results in release of nitric oxide by chondrocytes, activation of the NF-kappaB transcription factor and thus, expression of several pro-inflammatory cytokines.</csml:comment>
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PMID: 17959357, 15814732
Recognition of the urate crystals by TLR-2 and TLR-4 results in release of nitric oxide by chondrocytes, activation of the NF-kappaB transcription factor and thus, expression of several pro-inflammatory cytokines.</csml:comment>
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PMID: 17959357, 16670522
In the murine model of experimental colitis, TLR-9 signaling may inhibit colonic inflammation via production of type I interferons and the distinctive apical TLR-9 expression and signaling in intestinal epithelial cells is important for the maintenance of colonic homeostasis.</csml:comment>
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PMID: 17959357, 17114417
In this context, TLR-3 stimulation of antigen-presenting cells by the ds-RNA analog poly I:C was able to suppress relapsing demyelination in a murine experimental encephalomyelitis (EAE) model by inducing endogenous IFN-beta.</csml:comment>
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PMID: 17959357, 17114417
In this context, TLR-3 stimulation of antigen-presenting cells by the ds-RNA analog poly I:C was able to suppress relapsing demyelination in a murine experimental encephalomyelitis (EAE) model by inducing endogenous IFN-beta.</csml:comment>
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PMID: 17959357, 15611427
Although less thoroughly studied, an important role for TLR signaling has been documented in psoriasis. Local treatment with imiquimod (TLR-7 agonist) resulted in psoriasis exacerbation, which was attributed to the TLR-7 mediated IFN-alpha production by local pDCs.</csml:comment>
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PMID: 17959357, 15611427
Although less thoroughly studied, an important role for TLR signaling has been documented in psoriasis. Local treatment with imiquimod (TLR-7 agonist) resulted in psoriasis exacerbation, which was attributed to the TLR-7 mediated IFN-alpha production by local pDCs.</csml:comment>
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PMID: 17959357, 15948188
In cultures of human microglia, ligation of TLR3 and TLR4 by double-stranded RNA and LPS, respectively, induces the secretion of the chemokine CXCL10, which is a potent chemoattractant for T cells and is implicated in playing an important role in the MS lesion.</csml:comment>
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PMID: 17959357, 15948188
In cultures of human microglia, ligation of TLR3 and TLR4 by double-stranded RNA and LPS, respectively, induces the secretion of the chemokine CXCL10, which is a potent chemoattractant for T cells and is implicated in playing an important role in the MS lesion.</csml:comment>
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PMID: 17959357, 16955143
Toll-like receptor 3 mediated activation of macrophages and DCs by LCMV virus, resulting in an increased IFN-alpha and TNF-alpha secretion and thus, self reactive CD8+ cell recruitment has been implicated in the pathogenesis of mouse autoimmune hepatitis.</csml:comment>
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PMID: 17959357, 16955143
Toll-like receptor 3 mediated activation of macrophages and DCs by LCMV virus, resulting in an increased IFN-alpha and TNF-alpha secretion and thus, self reactive CD8+ cell recruitment has been implicated in the pathogenesis of mouse autoimmune hepatitis.</csml:comment>
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