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association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

{"project":"bionlp-st-ge-2016-coref","denotations":[{"id":"T23328","span":{"begin":610,"end":614},"obj":"Antecedent"},{"id":"T23327","span":{"begin":646,"end":652},"obj":"Anaphor"},{"id":"T23326","span":{"begin":332,"end":344},"obj":"Antecedent"},{"id":"T23325","span":{"begin":300,"end":326},"obj":"Antecedent"},{"id":"T23324","span":{"begin":293,"end":298},"obj":"Antecedent"},{"id":"T23323","span":{"begin":287,"end":291},"obj":"Antecedent"},{"id":"T23322","span":{"begin":256,"end":280},"obj":"Anaphor"},{"id":"T23321","span":{"begin":256,"end":280},"obj":"Antecedent"},{"id":"T23320","span":{"begin":220,"end":242},"obj":"Anaphor"}],"relations":[{"id":"R11368","pred":"boundBy","subj":"T23320","obj":"T23321"},{"id":"R11369","pred":"boundBy","subj":"T23321","obj":"T23323"},{"id":"R11370","pred":"boundBy","subj":"T23321","obj":"T23324"},{"id":"R11371","pred":"boundBy","subj":"T23321","obj":"T23325"},{"id":"R11372","pred":"boundBy","subj":"T23321","obj":"T23326"},{"id":"R11373","pred":"boundBy","subj":"T23327","obj":"T23328"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"In association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T23442","span":{"begin":1283,"end":1288},"obj":"Protein"},{"id":"T23441","span":{"begin":1213,"end":1216},"obj":"Protein"},{"id":"T23440","span":{"begin":1195,"end":1200},"obj":"Protein"},{"id":"T23439","span":{"begin":1130,"end":1135},"obj":"Protein"},{"id":"T23438","span":{"begin":1104,"end":1107},"obj":"Protein"},{"id":"T23437","span":{"begin":1054,"end":1059},"obj":"Protein"},{"id":"T23436","span":{"begin":1014,"end":1018},"obj":"Protein"},{"id":"T23435","span":{"begin":923,"end":926},"obj":"Protein"},{"id":"T23434","span":{"begin":894,"end":899},"obj":"Protein"},{"id":"T23433","span":{"begin":855,"end":860},"obj":"Protein"},{"id":"T23432","span":{"begin":803,"end":807},"obj":"Protein"},{"id":"T23423","span":{"begin":293,"end":298},"obj":"Protein"},{"id":"T23422","span":{"begin":287,"end":291},"obj":"Protein"},{"id":"T23421","span":{"begin":198,"end":203},"obj":"Protein"},{"id":"T23420","span":{"begin":167,"end":170},"obj":"Protein"},{"id":"T23419","span":{"begin":62,"end":67},"obj":"Protein"},{"id":"T23418","span":{"begin":44,"end":49},"obj":"Protein"},{"id":"T23417","span":{"begin":29,"end":34},"obj":"Protein"},{"id":"T23431","span":{"begin":756,"end":759},"obj":"Protein"},{"id":"T23430","span":{"begin":725,"end":730},"obj":"Protein"},{"id":"T23429","span":{"begin":629,"end":634},"obj":"Protein"},{"id":"T23428","span":{"begin":610,"end":614},"obj":"Protein"},{"id":"T23427","span":{"begin":412,"end":416},"obj":"Protein"},{"id":"T23426","span":{"begin":381,"end":386},"obj":"Protein"},{"id":"T23425","span":{"begin":332,"end":344},"obj":"Protein"},{"id":"T23424","span":{"begin":300,"end":326},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"In association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T26426","span":{"begin":1014,"end":1018},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T26425","span":{"begin":803,"end":807},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T26424","span":{"begin":610,"end":614},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T26423","span":{"begin":412,"end":416},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T26422","span":{"begin":287,"end":291},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T26421","span":{"begin":256,"end":260},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T26404","span":{"begin":1054,"end":1059},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T26403","span":{"begin":855,"end":860},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T26402","span":{"begin":629,"end":634},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T26401","span":{"begin":198,"end":203},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T26400","span":{"begin":62,"end":67},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T26399","span":{"begin":44,"end":49},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T26360","span":{"begin":1283,"end":1288},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T26359","span":{"begin":1195,"end":1200},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T26358","span":{"begin":1130,"end":1135},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T26357","span":{"begin":894,"end":899},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T26356","span":{"begin":725,"end":730},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T26355","span":{"begin":381,"end":386},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T26354","span":{"begin":29,"end":34},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T24250","span":{"begin":1213,"end":1216},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T24249","span":{"begin":1104,"end":1107},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T24248","span":{"begin":923,"end":926},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T24247","span":{"begin":756,"end":759},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T24246","span":{"begin":167,"end":170},"obj":"http://www.uniprot.org/uniprot/P01730"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"In association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

{"project":"UBERON-AE","denotations":[{"id":"T22794","span":{"begin":1008,"end":1013},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"T22793","span":{"begin":670,"end":675},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"T22791","span":{"begin":557,"end":562},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"}],"text":"In association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

{"project":"GO-BP","denotations":[{"id":"T22910","span":{"begin":1136,"end":1145},"obj":"http://purl.obolibrary.org/obo/GO_0046903"},{"id":"T22909","span":{"begin":1130,"end":1145},"obj":"http://purl.obolibrary.org/obo/GO_2001179"},{"id":"T22908","span":{"begin":1130,"end":1145},"obj":"http://purl.obolibrary.org/obo/GO_0072608"},{"id":"T22907","span":{"begin":557,"end":574},"obj":"http://purl.obolibrary.org/obo/GO_0008015"},{"id":"T22905","span":{"begin":350,"end":356},"obj":"http://purl.obolibrary.org/obo/GO_0040007"}],"text":"In association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

{"project":"GO-CC","denotations":[{"id":"T23672","span":{"begin":1220,"end":1225},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T23671","span":{"begin":1111,"end":1116},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T23670","span":{"begin":930,"end":935},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T23669","span":{"begin":763,"end":768},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T23668","span":{"begin":174,"end":179},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"In association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

{"project":"GO-MF","denotations":[{"id":"T23624","span":{"begin":332,"end":344},"obj":"http://purl.obolibrary.org/obo/GO_0005147"},{"id":"T23623","span":{"begin":293,"end":298},"obj":"http://purl.obolibrary.org/obo/GO_0005142"},{"id":"T23608","span":{"begin":1014,"end":1018},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T23607","span":{"begin":803,"end":807},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T23606","span":{"begin":610,"end":614},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T23605","span":{"begin":412,"end":416},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T23604","span":{"begin":287,"end":291},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T23603","span":{"begin":256,"end":260},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T23580","span":{"begin":1283,"end":1288},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T23579","span":{"begin":1195,"end":1200},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T23578","span":{"begin":1130,"end":1135},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T23577","span":{"begin":894,"end":899},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T23576","span":{"begin":725,"end":730},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T23575","span":{"begin":381,"end":386},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T23574","span":{"begin":29,"end":34},"obj":"http://purl.obolibrary.org/obo/GO_0005141"}],"text":"In association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

{"project":"sentences","denotations":[{"id":"T22827","span":{"begin":1020,"end":1294},"obj":"Sentence"},{"id":"T22826","span":{"begin":809,"end":1019},"obj":"Sentence"},{"id":"T22825","span":{"begin":581,"end":808},"obj":"Sentence"},{"id":"T22824","span":{"begin":392,"end":580},"obj":"Sentence"},{"id":"T22823","span":{"begin":198,"end":391},"obj":"Sentence"},{"id":"T22822","span":{"begin":0,"end":197},"obj":"Sentence"},{"id":"T165","span":{"begin":0,"end":197},"obj":"Sentence"},{"id":"T166","span":{"begin":198,"end":391},"obj":"Sentence"},{"id":"T167","span":{"begin":392,"end":580},"obj":"Sentence"},{"id":"T168","span":{"begin":581,"end":808},"obj":"Sentence"},{"id":"T169","span":{"begin":809,"end":1019},"obj":"Sentence"},{"id":"T170","span":{"begin":1020,"end":1294},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"In association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

{"project":"simple1","denotations":[{"id":"T24384","span":{"begin":1283,"end":1288},"obj":"Protein"},{"id":"T24383","span":{"begin":1213,"end":1216},"obj":"Protein"},{"id":"T24382","span":{"begin":1195,"end":1200},"obj":"Protein"},{"id":"T24381","span":{"begin":1130,"end":1135},"obj":"Protein"},{"id":"T24380","span":{"begin":1104,"end":1107},"obj":"Protein"},{"id":"T24379","span":{"begin":1054,"end":1059},"obj":"Protein"},{"id":"T24378","span":{"begin":1014,"end":1018},"obj":"Protein"},{"id":"T24377","span":{"begin":923,"end":926},"obj":"Protein"},{"id":"T24376","span":{"begin":894,"end":899},"obj":"Protein"},{"id":"T24375","span":{"begin":855,"end":860},"obj":"Protein"},{"id":"T24374","span":{"begin":803,"end":807},"obj":"Protein"},{"id":"T24373","span":{"begin":756,"end":759},"obj":"Protein"},{"id":"T24372","span":{"begin":725,"end":730},"obj":"Protein"},{"id":"T24371","span":{"begin":629,"end":634},"obj":"Protein"},{"id":"T24370","span":{"begin":610,"end":614},"obj":"Protein"},{"id":"T24369","span":{"begin":412,"end":416},"obj":"Protein"},{"id":"T24368","span":{"begin":381,"end":386},"obj":"Protein"},{"id":"T24367","span":{"begin":332,"end":344},"obj":"Protein"},{"id":"T24366","span":{"begin":300,"end":326},"obj":"Protein"},{"id":"T24365","span":{"begin":293,"end":298},"obj":"Protein"},{"id":"T24364","span":{"begin":287,"end":291},"obj":"Protein"},{"id":"T24363","span":{"begin":198,"end":203},"obj":"Protein"},{"id":"T24362","span":{"begin":167,"end":170},"obj":"Protein"},{"id":"T24361","span":{"begin":62,"end":67},"obj":"Protein"},{"id":"T24360","span":{"begin":44,"end":49},"obj":"Protein"},{"id":"T24359","span":{"begin":29,"end":34},"obj":"Protein"}],"text":"In association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

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association with impaired IL-10-mediated STAT3 activation, STAT3 was found to be tyrosine phosphorylated persistently (up to 6 hours) in freshly isolated PB and ST CD4+ T cells from RA patients. STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

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STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}

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STAT3 is activated by a variety of cytokines, notably the IL-6 family of cytokines (e.g. IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) and growth factors, in addition to IL-10 [4]. Of these cytokines, IL-6 plays a predominant role in eliciting a systemic reaction such as the acute phase response in active RA, due mainly to its abundance in the blood circulation [27]. Consistent with this notion, IL-6 was the major STAT3-activating factor contained in the serum of active RA patients, and the responsiveness to IL-10 was suppressed in normal CD4+ T cells after 36 hours of incubation with IL-6. These results suggest that both the sustained STAT3 activation and the resistance to IL-10 inhibition found in RA CD4+ T cells may be induced after chronic exposure in vivo to high concentrations of serum IL-6. However, it is also possible that STAT3 activity could be constitutively induced in CD4+ T cells by their own IL-10 secretion, leading to the loss of sensitivity to exogenous IL-10, because RA CD4+ T cells in the ST are capable of producing significant levels of IL-10 [34]."}