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PMID: 14552837
Consistent with this, the proliferative response of bone-marrow-derived macrophages (BMMs) to colony-stimulating factor 1 [CSF1 or macrophage colony-stimulating factor (M-CSF)] was increased in IFNAR1&#8722;/&#8722; cells, as expected from the removal of an inhibitor of proliferation.</csml:comment>
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PMID: 14552837, 8783497
Furthermore, IFN-beta itself can regulate the differentiation or activation of almost all effector cells of the immune system, including B cells and DCs.</csml:comment>
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PMID: 14552837, 8783497, 8658169, 10871875
It can polarize the immune response towards a T helper 1 (Th1) response [27], promote survival of memory T cells [28] and prevent T-cell apoptosis (which could be responsible for persistent T-cell infiltrates in chronic inflammation, such as rheumatoid arthritis).</csml:comment>
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PMID: 14552837, 9851930, 10201887
The prototype PAMP is lipopolysaccharide (LPS), a surface component of Gram-negative bacteria, which activates TLR4.</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837, 11257452
LPS effects are mediated by the products of TLR response genes (TRGs), such as inducible nitric oxide synthase (NOS2), which generates microbicidal nitric oxide (NO) and cytokines such as interleukin-6 (IL-6), tumor necrosis factor-greek small letter alpha (TNF-alpha), interferons (IFNs) and chemokines.</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837, 11257452
LPS effects are mediated by the products of TLR response genes (TRGs), such as inducible nitric oxide synthase (NOS2), which generates microbicidal nitric oxide (NO) and cytokines such as interleukin-6 (IL-6), tumor necrosis factor-greek small letter alpha (TNF-alpha), interferons (IFNs) and chemokines.</csml:comment>
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PMID: 14552837, 11477402, 12072368
LPS activation of TLR4 signaling triggers the recruitment of the adaptor molecule MyD88 through their Toll&#8211;IL-1 receptor (TIR) domains.

PMID: 14552837, 11544529, 11526399
The MyD88 adaptor-like (Mal) protein [38], also known as TIR-containing adaptor protein (TIRAP) [39], was discovered as a TIR-domain-containing adaptor that, unlike MyD88, does not have a death domain.</csml:comment>
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PMID: 14552837
This is followed by the recruitment and activation of IRAK and TRAF6.</csml:comment>
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PMID: 14552837
This is followed by the recruitment and activation of IRAK and TRAF6.</csml:comment>
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PMID: 14552837
This is followed by the recruitment and activation of IRAK and TRAF6.</csml:comment>
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PMID: 14552837
This is followed by the recruitment and activation of IRAK and TRAF6.</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID: 14552837
This is followed by the recruitment and activation of IRAK and TRAF6.</csml:comment>
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</csml:process>
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<csml:comment type="text">

</csml:comment>
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Indirect</csml:comment>
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<csml:comment type="text">

</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID: 14552837
This results in the activation of both the MAP kinases and NF-kappaB.</csml:comment>
</csml:comments>
</csml:process>
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Indirect</csml:comment>
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Indirect</csml:comment>
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</csml:comment>
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<csml:comment type="text">


PMID: 14552837, 11257452
LPS effects are mediated by the products of TLR response genes (TRGs), such as inducible nitric oxide synthase (NOS2), which generates microbicidal nitric oxide (NO) and cytokines such as interleukin-6 (IL-6), tumor necrosis factor-greek small letter alpha (TNF-alpha), interferons (IFNs) and chemokines.</csml:comment>
</csml:comments>
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<csml:comments>
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Indirect</csml:comment>
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Indirect</csml:comment>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID: 14552837, 11257452
LPS effects are mediated by the products of TLR response genes (TRGs), such as inducible nitric oxide synthase (NOS2), which generates microbicidal nitric oxide (NO) and cytokines such as interleukin-6 (IL-6), tumor necrosis factor-greek small letter alpha (TNF-alpha), interferons (IFNs) and chemokines.</csml:comment>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
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<csml:comments>
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Indirect</csml:comment>
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</csml:connector>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
</csml:connector>
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<csml:toolSpecificGraphics/>
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<csml:comments>
<csml:comment type="text">


PMID: 14552837
This results in the activation of both the MAP kinases and NF-kappaB.

PMID: 14552837
Recent studies demonstrated that IKbeta kinases, previously known to be involved in NF-kappaB activation, are essential for activation of IRF3 and 7.</csml:comment>
</csml:comments>
</csml:process>
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<csml:connector id="c26" name="c26" refID="MO000022224" type="cso30:c:InputProcess">
<csml:connectorSimulationProperty>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
</csml:connector>
<csml:connector id="c40" name="c40" refID="MO000019398" type="cso30:c:InputProcess">
<csml:connectorSimulationProperty>
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PMID: 14552837, 12471095, 12539043
Although previous studies would lead us to interpret data from overexpression or dominant-negative experiments with caution, the data on TLR3 activation of IFN-beta by TRIF/TICAM, but not by MyD88 or Mal/TIRAP, is consistent between these studies.</csml:comment>
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PMID: 14552837, 12471095, 12539043
Although previous studies would lead us to interpret data from overexpression or dominant-negative experiments with caution, the data on TLR3 activation of IFN-beta by TRIF/TICAM, but not by MyD88 or Mal/TIRAP, is consistent between these studies.</csml:comment>
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PMID: 14552837, 12471095, 12539043
Although previous studies would lead us to interpret data from overexpression or dominant-negative experiments with caution, the data on TLR3 activation of IFN-beta by TRIF/TICAM, but not by MyD88 or Mal/TIRAP, is consistent between these studies.

PMID: 14552837
However, in response to double-stranded RNA (poly I:C) activation of a related TLR3 receptor, the TRIF&#8211;TIR-containing adaptor molecule (TICAM) leads to IRF3 activation.

</csml:comment>
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PMID: 14552837, 12471095, 12539043
Although previous studies would lead us to interpret data from overexpression or dominant-negative experiments with caution, the data on TLR3 activation of IFN-beta by TRIF/TICAM, but not by MyD88 or Mal/TIRAP, is consistent between these studies.

PMID: 14552837
First, activation of IRF3 generated IFN-beta and -alpha4.

PMID: 14552837, 11698465
Recent analyses of TLR signaling have identified the LPS induction of additional IFN response genes (IRGs), including IFN-gamma-inducible protein 10 (IP-10), monocyte chemotactic protein 5 (MCP-5), RANTES and IFN-stimulated gene 15 (ISG15), as well as IFN-beta through a so-called MyD88-independent pathway.</csml:comment>
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</csml:comment>
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<csml:comment type="text">


PMID: 14552837
First, activation of IRF3 generated IFN-beta and -alpha4.</csml:comment>
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</csml:comment>
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PMID: 14552837
These acted through their cognate receptors, IFNAR1 and IFNAR2, to activate STAT1 to induce IRF7.</csml:comment>
</csml:comments>
</csml:process>
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PMID: 14552837
These acted through their cognate receptors, IFNAR1 and IFNAR2, to activate STAT1 to induce IRF7.</csml:comment>
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Indirect</csml:comment>
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<csml:comment type="text">


PMID: 14552837
These acted through their cognate receptors, IFNAR1 and IFNAR2, to activate STAT1 to induce IRF7.</csml:comment>
</csml:comments>
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Indirect</csml:comment>
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<csml:comment type="text">


PMID: 14552837
These acted through their cognate receptors, IFNAR1 and IFNAR2, to activate STAT1 to induce IRF7.</csml:comment>
</csml:comments>
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Indirect</csml:comment>
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<csml:comment type="text">


PMID: 14552837
These acted through their cognate receptors, IFNAR1 and IFNAR2, to activate STAT1 to induce IRF7.</csml:comment>
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</csml:comment>
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<csml:comment type="text">


PMID: 14552837
Activation of IRF7 then induced the remaining IFN-alpha subtype.</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837
Recent studies demonstrated that IKbeta kinases, previously known to be involved in NF-kappaB activation, are essential for activation of IRF3 and 7.</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837
Recent studies demonstrated that IKbeta kinases, previously known to be involved in NF-kappaB activation, are essential for activation of IRF3 and 7.</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837, 12062447
Similar studies indicated that Mal was necessary for the activation of IRF3 by LPS but not by poly I:C.</csml:comment>
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PMID: 14552837
Consistent with this, the proliferative response of bone-marrow-derived macrophages (BMMs) to colony-stimulating factor 1 [CSF1 or macrophage colony-stimulating factor (M-CSF)] was increased in IFNAR1&#8722;/&#8722; cells, as expected from the removal of an inhibitor of proliferation.</csml:comment>
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Indirect</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837, 11052814
We then demonstrated that LPS induction of NOS2 [22] and cyclin D2 [23] was also absent in IFNAR1&#8722;/&#8722; cells.</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837, 11698465
Recent analyses of TLR signaling have identified the LPS induction of additional IFN response genes (IRGs), including IFN-gamma-inducible protein 10 (IP-10), monocyte chemotactic protein 5 (MCP-5), RANTES and IFN-stimulated gene 15 (ISG15), as well as IFN-beta through a so-called MyD88-independent pathway.</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837, 11698465
Recent analyses of TLR signaling have identified the LPS induction of additional IFN response genes (IRGs), including IFN-gamma-inducible protein 10 (IP-10), monocyte chemotactic protein 5 (MCP-5), RANTES and IFN-stimulated gene 15 (ISG15), as well as IFN-beta through a so-called MyD88-independent pathway.</csml:comment>
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Indirect</csml:comment>
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Indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">

PMID: 14552837, 11698465
Recent analyses of TLR signaling have identified the LPS induction of additional IFN response genes (IRGs), including IFN-gamma-inducible protein 10 (IP-10), monocyte chemotactic protein 5 (MCP-5), RANTES and IFN-stimulated gene 15 (ISG15), as well as IFN-beta through a so-called MyD88-independent pathway.</csml:comment>
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PMID: 14552837
IFN-gamma is produced predominantly by T cells, natural killer (NK) cells and NKT cells in response to mitogens or cytokines (e.g. IL-12).</csml:comment>
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Indirect</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837
IFN-gamma is produced predominantly by T cells, natural killer (NK) cells and NKT cells in response to mitogens or cytokines (e.g. IL-12).</csml:comment>
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Indirect</csml:comment>
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Indirect</csml:comment>
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<csml:comment type="text">

PMID: 14552837, 11477402
Not only is the TLR response the cornerstone of innate immunity but the products of TLR signaling (e.g. IFNs, IL-12) also shape the adaptive immune response.</csml:comment>
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PMID: 14552837, 11477402
Not only is the TLR response the cornerstone of innate immunity but the products of TLR signaling (e.g. IFNs, IL-12) also shape the adaptive immune response.</csml:comment>
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PMID: 14552837
Although the rapidity of the effect of SOCS in vitro and the association with IRAK suggested that there was a direct effect of SOCS on TLR signaling.</csml:comment>
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Indirect</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837, 12433365, 12433373, 10453004
SOCS are induced after activation of TLR4 [51 and 52] and TLR9[50].</csml:comment>
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Indirect</csml:comment>
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Indirect</csml:comment>
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PMID: 14552837, 12433365, 12433373, 10453004
SOCS are induced after activation of TLR4 [51 and 52] and TLR9[50].</csml:comment>
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PMID: 14552837
Activation of IRF7 then induced the remaining IFN-alpha subtype.</csml:comment>
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PMID: 14552837
This results in the activation of both the MAP kinases and NF-kappaB.

PMID: 14552837
Recent studies demonstrated that IKbeta kinases, previously known to be involved in NF-kappaB activation, are essential for activation of IRF3 and 7.</csml:comment>
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