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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
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PMID: 15886111
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PMID: 15886111
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PMID: 15886111
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PMID: 15886111
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.

PMID: 15886111, 12689944 , 12560217
B cells are now particularly well recognized for their expression of the TLR9 and TLR10, which are induced in response to BCR stimulation and appear to predominate in activated and/or memory populations.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.

PMID: 15886111, 12689944 , 12560217
B cells are now particularly well recognized for their expression of the TLR9 and TLR10, which are induced in response to BCR stimulation and appear to predominate in activated and/or memory populations.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Although most studies agree that mRNAs corresponding to all TLRs can be detected in B cells, significant expression is only generally agreed upon at this time for TLR1 and TLR6&#8211;10, all of which are upregulated during activation; for example, in response to B cell receptor (BCR) or CD40 ligation, CpG oligonucleotide exposure in vitro, and as seen in activated B cell subsets ex vivo.</csml:comment>
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PMID: 15886111
Extracellular lipopolysaccharide (LPS) is bound by LPS-binding protein (LBP), recognized by CD14, and brought in proximity to the TLR4&#8211;MD-2 and RP105&#8211;MD-1 heterodimers.</csml:comment>
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PMID: 15886111
Extracellular lipopolysaccharide (LPS) is bound by LPS-binding protein (LBP), recognized by CD14, and brought in proximity to the TLR4&#8211;MD-2 and RP105&#8211;MD-1 heterodimers.</csml:comment>
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PMID: 15886111
TLR4 initiates signaling via at least two adaptor pathways: TIRAP&#8211;MyD88 and TRIF&#8211;TRAM.</csml:comment>
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PMID: 15886111
Extracellular lipopolysaccharide (LPS) is bound by LPS-binding protein (LBP), recognized by CD14, and brought in proximity to the TLR4&#8211;MD-2 and RP105&#8211;MD-1 heterodimers.</csml:comment>
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Indirect</csml:comment>
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PMID: 15886111, 14707068
This spectrum of inducible expression of the TLRs has been generally presumed to extend to rodent B cells; however, species differences clearly exist, as na&#239;ve murine B cells are known to express TLR4 and undergo proliferation and plasmacytoid differentiation in vitro in response to LPS exposure, in contrast to human B cells, which seem to lack significant TLR4 expression, at least in the na&#239;ve resting state.</csml:comment>
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Indirect</csml:comment>
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PMID: 15886111, 14707068
This spectrum of inducible expression of the TLRs has been generally presumed to extend to rodent B cells; however, species differences clearly exist, as na&#239;ve murine B cells are known to express TLR4 and undergo proliferation and plasmacytoid differentiation in vitro in response to LPS exposure, in contrast to human B cells, which seem to lack significant TLR4 expression, at least in the na&#239;ve resting state.

PMID: 15886111
Both the NF-kappaB and AP-1 proteins enter the nucleus where they activate target genes involved in B cell activation, proliferation, and immunoglobulin (Ig) production.</csml:comment>
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PMID: 15886111, 14707068
This spectrum of inducible expression of the TLRs has been generally presumed to extend to rodent B cells; however, species differences clearly exist, as na&#239;ve murine B cells are known to express TLR4 and undergo proliferation and plasmacytoid differentiation in vitro in response to LPS exposure, in contrast to human B cells, which seem to lack significant TLR4 expression, at least in the na&#239;ve resting state.

PMID: 15886111
Both the NF-kappaB and AP-1 proteins enter the nucleus where they activate target genes involved in B cell activation, proliferation, and immunoglobulin (Ig) production.</csml:comment>
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PMID: 15886111
TLR4 initiates signaling via at least two adaptor pathways: TIRAP&#8211;MyD88 and TRIF&#8211;TRAM.</csml:comment>
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PMID: 15886111
The TIRAP&#8211;MyD88 pathway elicits an IRAK&#8211;TRAF6&#8211;TAK1 pathway.

PMID: 15886111
TAK1 activates NIK, which activates the IKK complex, which in turn phosphorylates the IkappaB proteins that normally sequester NF-kappaB proteins in the cytoplasm.</csml:comment>
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PMID: 15886111
TAK1 activates NIK, which activates the IKK complex, which in turn phosphorylates the IkappaB proteins that normally sequester NF-kappaB proteins in the cytoplasm.</csml:comment>
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PMID: 15886111
TAK1 activates NIK, which activates the IKK complex, which in turn phosphorylates the IkappaB proteins that normally sequester NF-kappaB proteins in the cytoplasm.</csml:comment>
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PMID: 15886111
TAK1 activates NIK, which activates the IKK complex, which in turn phosphorylates the IkappaB proteins that normally sequester NF-kappaB proteins in the cytoplasm.</csml:comment>
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PMID: 15886111
TAK1 activates NIK, which activates the IKK complex, which in turn phosphorylates the IkappaB proteins that normally sequester NF-kappaB proteins in the cytoplasm.

PMID: 15886111
Together, these kinases result in both IkappaB phosphorylation and NF-kappaB activation, enhancing the transcription of inflammatory cytokines, as well as the activation of STAT1 and IRF-3, which regulate the expression of IFN-inducible genes.</csml:comment>
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PMID: 15886111
TAK1 also activates the JNK and p38 MAPK pathways, leading to the activation of AP-1 complexes.</csml:comment>
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PMID: 15886111
TAK1 also activates the JNK and p38 MAPK pathways, leading to the activation of AP-1 complexes.</csml:comment>
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PMID: 15886111
TAK1 also activates the JNK and p38 MAPK pathways, leading to the activation of AP-1 complexes.</csml:comment>
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PMID: 15886111
TAK1 also activates the JNK and p38 MAPK pathways, leading to the activation of AP-1 complexes.</csml:comment>
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PMID: 15886111
TAK1 also activates the JNK and p38 MAPK pathways, leading to the activation of AP-1 complexes.</csml:comment>
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PMID: 15886111
TAK1 also activates the JNK and p38 MAPK pathways, leading to the activation of AP-1 complexes.</csml:comment>
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PMID: 15886111
Both the NF-kappaB and AP-1 proteins enter the nucleus where they activate target genes involved in inflammation, particularly cytokines.

PMID: 15886111
Together, these kinases result in both IkappaB phosphorylation and NF-kappaB activation, enhancing the transcription of inflammatory cytokines, as well as the activation of STAT1 and IRF-3, which regulate the expression of IFN-inducible genes.</csml:comment>
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PMID: 15886111
Both the NF-kappaB and AP-1 proteins enter the nucleus where they activate target genes involved in inflammation, particularly cytokines.</csml:comment>
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Indirect</csml:comment>
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PMID: 15886111
Both the NF-kappaB and AP-1 proteins enter the nucleus where they activate target genes involved in inflammation, particularly cytokines.</csml:comment>
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Indirect</csml:comment>
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PMID: 15886111
Both the NF-kappaB and AP-1 proteins enter the nucleus where they activate target genes involved in inflammation, particularly cytokines.</csml:comment>
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Indirect</csml:comment>
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PMID: 15886111, 14745443
The TRIF&#8211;TRAM pathway results in activation of the atypical IKKs IKK-epsilon and TBK1, as well as the IFN-inducible PKR.</csml:comment>
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PMID: 15886111, 14745443
The TRIF&#8211;TRAM pathway results in activation of the atypical IKKs IKK-epsilon and TBK1, as well as the IFN-inducible PKR.</csml:comment>
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PMID: 15886111
Together, these kinases result in both IkappaB phosphorylation and NF-kappaB activation, enhancing the transcription of inflammatory cytokines, as well as the activation of STAT1 and IRF-3, which regulate the expression of IFN-inducible genes.</csml:comment>
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PMID: 15886111, 14745443
The TRIF&#8211;TRAM pathway results in activation of the atypical IKKs IKK-epsilon and TBK1, as well as the IFN-inducible PKR.</csml:comment>
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PMID: 15886111
Together, these kinases result in both IkappaB phosphorylation and NF-kappaB activation, enhancing the transcription of inflammatory cytokines, as well as the activation of STAT1 and IRF-3, which regulate the expression of IFN-inducible genes.</csml:comment>
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PMID: 15886111
Together, these kinases result in both IkappaB phosphorylation and NF-kappaB activation, enhancing the transcription of inflammatory cytokines, as well as the activation of STAT1 and IRF-3, which regulate the expression of IFN-inducible genes.</csml:comment>
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PMID: 15886111, 11948342
For instance, anti-DNA IgG autoantibodies can form complexes with hypomethylated CpG-containing DNAs, and then bind both to rheumatoid factor (anti-IgG) B cells through their BCR via direct IgG binding, and to TLR9 via binding of the co-complexed DNA, resulting in activation.</csml:comment>
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PMID: 15886111, 11948342
For instance, anti-DNA IgG autoantibodies can form complexes with hypomethylated CpG-containing DNAs, and then bind both to rheumatoid factor (anti-IgG) B cells through their BCR via direct IgG binding, and to TLR9 via binding of the co-complexed DNA, resulting in activation.

PMID: 15886111
Environmental CpG-containing DNAs (mammalian or non-mammalian) are directly endocytosed or internalized after binding to anti-DNA BCRs.</csml:comment>
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PMID: 15886111, 11948342
For instance, anti-DNA IgG autoantibodies can form complexes with hypomethylated CpG-containing DNAs, and then bind both to rheumatoid factor (anti-IgG) B cells through their BCR via direct IgG binding, and to TLR9 via binding of the co-complexed DNA, resulting in activation.</csml:comment>
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PMID: 15886111
Together, these kinases result in both IkappaB phosphorylation and NF-kappaB activation, enhancing the transcription of inflammatory cytokines, as well as the activation of STAT1 and IRF-3, which regulate the expression of IFN-inducible genes.</csml:comment>
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PMID: 15886111
Together, these kinases result in both IkappaB phosphorylation and NF-kappaB activation, enhancing the transcription of inflammatory cytokines, as well as the activation of STAT1 and IRF-3, which regulate the expression of IFN-inducible genes.</csml:comment>
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PMID: 15886111
TLR9, normally generated and found in the endoplasmic reticulum, encounters CpG DNAs in lysosomal/late endosomal compartments, where it initiates a signaling cascade via MyD88&#8211;IRAK&#8211;TRAF6&#8211;TAK1, similar to TLR4 (Figure 1 but without TIRAP.</csml:comment>
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PMID: 15886111
TLR9, normally generated and found in the endoplasmic reticulum, encounters CpG DNAs in lysosomal/late endosomal compartments, where it initiates a signaling cascade via MyD88&#8211;IRAK&#8211;TRAF6&#8211;TAK1, similar to TLR4 (Figure 1 but without TIRAP.</csml:comment>
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PMID: 15886111
TLR9, normally generated and found in the endoplasmic reticulum, encounters CpG DNAs in lysosomal/late endosomal compartments, where it initiates a signaling cascade via MyD88&#8211;IRAK&#8211;TRAF6&#8211;TAK1, similar to TLR4 (Figure 1 but without TIRAP.</csml:comment>
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PMID: 15886111
TLR9, normally generated and found in the endoplasmic reticulum, encounters CpG DNAs in lysosomal/late endosomal compartments, where it initiates a signaling cascade via MyD88&#8211;IRAK&#8211;TRAF6&#8211;TAK1, similar to TLR4 (Figure 1 but without TIRAP.</csml:comment>
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PMID: 15886111
TLR9, normally generated and found in the endoplasmic reticulum, encounters CpG DNAs in lysosomal/late endosomal compartments, where it initiates a signaling cascade via MyD88&#8211;IRAK&#8211;TRAF6&#8211;TAK1, similar to TLR4 (Figure 1 but without TIRAP.</csml:comment>
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PMID: 15886111
Both the NF-kappaB and AP-1 proteins enter the nucleus where they activate target genes involved in B cell activation, proliferation, and immunoglobulin (Ig) production.</csml:comment>
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PMID: 15886111
Both the NF-kappaB and AP-1 proteins enter the nucleus where they activate target genes involved in B cell activation, proliferation, and immunoglobulin (Ig) production.</csml:comment>
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PMID: 15886111
In such studies, CpG treatments are associated with the preferential production of &#8216;Th1-like&#8217; immunoglobulin isotypes, such as the IFN-gamma-related IgG2a in mice.

PMID: 15886111, 15114682, 14586416
Interestingly, the Th1-like effect requires the classical MyD88 adaptor pathway and, at least for IgG2a class switching, requires the Th1-related T-box transcription factor T-bet, but the effect of CpG DNAs on IgG1 and IgE production appears to be at least partially MyD88 independent.</csml:comment>
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PMID: 15886111
In such studies, CpG treatments are associated with the preferential production of &#8216;Th1-like&#8217; immunoglobulin isotypes, such as the IFN-gamma-related IgG2a in mice.

PMID: 15886111, 15114682, 14586416
Interestingly, the Th1-like effect requires the classical MyD88 adaptor pathway and, at least for IgG2a class switching, requires the Th1-related T-box transcription factor T-bet, but the effect of CpG DNAs on IgG1 and IgE production appears to be at least partially MyD88 independent.</csml:comment>
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PMID: 15886111, 15114682, 12766768, 14586416
Previously, such effects upon B cells were presumed to reflect the indirect effect of skewing towards and/or preferential survival of Th1 cells in the helper T cell compartment, but recent studies indicate that CpG DNAs might have direct effects upon murine B cells, inducing and/or promoting class switching to &#8216;Th1-like&#8217; isotypes, such as IgG2a, IgG2b and IgG3, while suppressing the production of the &#8216;Th2-like&#8217; (IL-4-related) isotypes IgG1 and IgE.</csml:comment>
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PMID: 15886111, 15114682, 12766768, 14586416
Previously, such effects upon B cells were presumed to reflect the indirect effect of skewing towards and/or preferential survival of Th1 cells in the helper T cell compartment, but recent studies indicate that CpG DNAs might have direct effects upon murine B cells, inducing and/or promoting class switching to &#8216;Th1-like&#8217; isotypes, such as IgG2a, IgG2b and IgG3, while suppressing the production of the &#8216;Th2-like&#8217; (IL-4-related) isotypes IgG1 and IgE.</csml:comment>
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PMID: 15886111, 15114682, 12766768, 14586416
Previously, such effects upon B cells were presumed to reflect the indirect effect of skewing towards and/or preferential survival of Th1 cells in the helper T cell compartment, but recent studies indicate that CpG DNAs might have direct effects upon murine B cells, inducing and/or promoting class switching to &#8216;Th1-like&#8217; isotypes, such as IgG2a, IgG2b and IgG3, while suppressing the production of the &#8216;Th2-like&#8217; (IL-4-related) isotypes IgG1 and IgE.</csml:comment>
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PMID: 15886111, 12778475, 15249208, 15070685
Other studies have indicated that, whereas CpG DNAs alone can induce the expression of co-stimulatory molecules and chemokine receptors such as CXCR3 in human B cells, CpG DNAs require synergistic cooperation with CD40 signals and/or simultaneous culture with plasmacytoid dendritic cells to induce secretion of immunoglobulins or cytokines such as IL-6 and IL-10, or to promote Th1 development by helper T cells</csml:comment>
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PMID: 15886111, 12778475, 15249208, 15070685
Other studies have indicated that, whereas CpG DNAs alone can induce the expression of co-stimulatory molecules and chemokine receptors such as CXCR3 in human B cells, CpG DNAs require synergistic cooperation with CD40 signals and/or simultaneous culture with plasmacytoid dendritic cells to induce secretion of immunoglobulins or cytokines such as IL-6 and IL-10, or to promote Th1 development by helper T cells</csml:comment>
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PMID: 15886111, 12778475, 15249208, 15070685
Other studies have indicated that, whereas CpG DNAs alone can induce the expression of co-stimulatory molecules and chemokine receptors such as CXCR3 in human B cells, CpG DNAs require synergistic cooperation with CD40 signals and/or simultaneous culture with plasmacytoid dendritic cells to induce secretion of immunoglobulins or cytokines such as IL-6 and IL-10, or to promote Th1 development by helper T cells</csml:comment>
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PMID: 15886111, 14707068
Other studies have indicated that, whereas CpG DNAs alone can induce the expression of co-stimulatory molecules and chemokine receptors such as CXCR3 in human B cells, CpG DNAs require synergistic cooperation with CD40 signals and/or simultaneous culture with plasmacytoid dendritic cells to induce secretion of immunoglobulins or cytokines such as IL-6 and IL-10, or to promote Th1 development by helper T cells</csml:comment>
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PMID: 15886111, 11823477
Other TLRs similarly seem likely to affect B cell function both in humans and rodents in vivo. TLR2 ligands, such as neisserial porins, lipoproteins and glycoinositolphospholipids, have been shown to activate B cells, generally acting as mitogens.</csml:comment>
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PMID: 15886111, 11841848
Furthermore, some studies have indicated that TLR4 expression can in fact be induced in human B cells by specific stimuli, such as IL-4.</csml:comment>
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PMID: 15886111, 11823477
Other TLRs similarly seem likely to affect B cell function both in humans and rodents in vivo. TLR2 ligands, such as neisserial porins, lipoproteins and glycoinositolphospholipids, have been shown to activate B cells, generally acting as mitogens.</csml:comment>
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PMID: 15886111, 11823477
Other TLRs similarly seem likely to affect B cell function both in humans and rodents in vivo. TLR2 ligands, such as neisserial porins, lipoproteins and glycoinositolphospholipids, have been shown to activate B cells, generally acting as mitogens.</csml:comment>
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PMID: 15886111, 14976261, 14976262, 15034168
Also, the TLR7-binding guanosine analogs can stimulate human B cells, suggesting that B cells can be stimulated by the physiological ligands of TLR7, the single-stranded RNAs.</csml:comment>
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Indirect</csml:comment>
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PMID: 15886111, 14971051, 15481148
For instance, species-specific differences in optimal CpG sequences suggest differential regulation and/or recognition of TLR9 binding and/or signaling, and it has become clear that several &#8216;classes&#8217; of stimulatory CpG oligonucleotides (ODNs) exist: CpG-A ODNs, which strongly induce IFN-&#945; in plasmacytoid dendritic cells (PDCs) and potently activate NK cells; CpG-B ODNs, which potently activate NK and B cells but not PDCs; and CpG-C ODNs, which combine the effects of both.</csml:comment>
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Indirect</csml:comment>
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PMID: 15886111, 14971051, 15481148
For instance, species-specific differences in optimal CpG sequences suggest differential regulation and/or recognition of TLR9 binding and/or signaling, and it has become clear that several &#8216;classes&#8217; of stimulatory CpG oligonucleotides (ODNs) exist: CpG-A ODNs, which strongly induce IFN-&#945; in plasmacytoid dendritic cells (PDCs) and potently activate NK cells; CpG-B ODNs, which potently activate NK and B cells but not PDCs; and CpG-C ODNs, which combine the effects of both.</csml:comment>
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PMID: 15886111
TAK1 also activates the JNK and p38 MAPK pathways, leading to the activation of AP-1 complexes.</csml:comment>
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PMID: 15886111
TAK1 also activates the JNK and p38 MAPK pathways, leading to the activation of AP-1 complexes.</csml:comment>
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