PubMed:27630165 JSON TXT

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LitCoin-entities

LitCoin-sentences

{"project":"LitCoin-sentences","denotations":[{"id":"T1","span":{"begin":0,"end":186},"obj":"Sentence"},{"id":"T2","span":{"begin":187,"end":349},"obj":"Sentence"},{"id":"T3","span":{"begin":350,"end":539},"obj":"Sentence"},{"id":"T4","span":{"begin":540,"end":903},"obj":"Sentence"},{"id":"T5","span":{"begin":904,"end":1120},"obj":"Sentence"},{"id":"T6","span":{"begin":1121,"end":1279},"obj":"Sentence"},{"id":"T7","span":{"begin":1280,"end":1410},"obj":"Sentence"},{"id":"T8","span":{"begin":1411,"end":1573},"obj":"Sentence"},{"id":"T9","span":{"begin":1574,"end":1732},"obj":"Sentence"},{"id":"T10","span":{"begin":1733,"end":2026},"obj":"Sentence"}],"text":"Long-Lived CD4+IFN-γ+ T Cells rather than Short-Lived CD4+IFN-γ+IL-10+ T Cells Initiate Rapid IL-10 Production To Suppress Anamnestic T Cell Responses during Secondary Malaria Infection.\nCD4(+) T cells that produce IFN-γ are the source of host-protective IL-10 during primary infection with a number of different pathogens, including Plasmodium spp. The fate of these CD4(+)IFN-γ(+)IL-10(+) T cells following clearance of primary infection and their subsequent influence on the course of repeated infections is, however, presently unknown. In this study, utilizing IFN-γ-yellow fluorescent protein (YFP) and IL-10-GFP dual reporter mice, we show that primary malaria infection-induced CD4(+)YFP(+)GFP(+) T cells have limited memory potential, do not stably express IL-10, and are disproportionately lost from the Ag-experienced CD4(+) T cell memory population during the maintenance phase postinfection. CD4(+)YFP(+)GFP(+) T cells generally exhibited a short-lived effector rather than effector memory T cell phenotype postinfection and expressed high levels of PD-1, Lag-3, and TIGIT, indicative of cellular exhaustion. Consistently, the surviving CD4(+)YFP(+)GFP(+) T cell-derived cells were unresponsive and failed to proliferate during the early phase of secondary infection. In contrast, CD4(+)YFP(+)GFP(-) T cell-derived cells expanded rapidly and upregulated IL-10 expression during secondary infection. Correspondingly, CD4(+) T cells were the major producers within an accelerated and amplified IL-10 response during the early stage of secondary malaria infection. Notably, IL-10 exerted quantitatively stronger regulatory effects on innate and CD4(+) T cell responses during primary and secondary infections, respectively. The results in this study significantly improve our understanding of the durability of IL-10-producing CD4(+) T cells postinfection and provide information on how IL-10 may contribute to optimized parasite control and prevention of immune-mediated pathology during repeated malaria infections."}

LitCoin-entities-OrganismTaxon-PD

{"project":"LitCoin-entities-OrganismTaxon-PD","denotations":[{"id":"T1","span":{"begin":334,"end":344},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":632,"end":636},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"NCBItxid:5820"},{"id":"A2","pred":"db_id","subj":"T1","obj":"NCBItxid:418103"},{"id":"A3","pred":"db_id","subj":"T3","obj":"NCBItxid:10095"},{"id":"A4","pred":"db_id","subj":"T3","obj":"NCBItxid:10088"}],"text":"Long-Lived CD4+IFN-γ+ T Cells rather than Short-Lived CD4+IFN-γ+IL-10+ T Cells Initiate Rapid IL-10 Production To Suppress Anamnestic T Cell Responses during Secondary Malaria Infection.\nCD4(+) T cells that produce IFN-γ are the source of host-protective IL-10 during primary infection with a number of different pathogens, including Plasmodium spp. The fate of these CD4(+)IFN-γ(+)IL-10(+) T cells following clearance of primary infection and their subsequent influence on the course of repeated infections is, however, presently unknown. In this study, utilizing IFN-γ-yellow fluorescent protein (YFP) and IL-10-GFP dual reporter mice, we show that primary malaria infection-induced CD4(+)YFP(+)GFP(+) T cells have limited memory potential, do not stably express IL-10, and are disproportionately lost from the Ag-experienced CD4(+) T cell memory population during the maintenance phase postinfection. CD4(+)YFP(+)GFP(+) T cells generally exhibited a short-lived effector rather than effector memory T cell phenotype postinfection and expressed high levels of PD-1, Lag-3, and TIGIT, indicative of cellular exhaustion. Consistently, the surviving CD4(+)YFP(+)GFP(+) T cell-derived cells were unresponsive and failed to proliferate during the early phase of secondary infection. In contrast, CD4(+)YFP(+)GFP(-) T cell-derived cells expanded rapidly and upregulated IL-10 expression during secondary infection. Correspondingly, CD4(+) T cells were the major producers within an accelerated and amplified IL-10 response during the early stage of secondary malaria infection. Notably, IL-10 exerted quantitatively stronger regulatory effects on innate and CD4(+) T cell responses during primary and secondary infections, respectively. The results in this study significantly improve our understanding of the durability of IL-10-producing CD4(+) T cells postinfection and provide information on how IL-10 may contribute to optimized parasite control and prevention of immune-mediated pathology during repeated malaria infections."}

LitCoin_Mondo

{"project":"LitCoin_Mondo","denotations":[{"id":"T1","span":{"begin":168,"end":175},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":659,"end":666},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":1555,"end":1562},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":2007,"end":2014},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005136"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005136"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005136"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0005136"}],"text":"Long-Lived CD4+IFN-γ+ T Cells rather than Short-Lived CD4+IFN-γ+IL-10+ T Cells Initiate Rapid IL-10 Production To Suppress Anamnestic T Cell Responses during Secondary Malaria Infection.\nCD4(+) T cells that produce IFN-γ are the source of host-protective IL-10 during primary infection with a number of different pathogens, including Plasmodium spp. The fate of these CD4(+)IFN-γ(+)IL-10(+) T cells following clearance of primary infection and their subsequent influence on the course of repeated infections is, however, presently unknown. In this study, utilizing IFN-γ-yellow fluorescent protein (YFP) and IL-10-GFP dual reporter mice, we show that primary malaria infection-induced CD4(+)YFP(+)GFP(+) T cells have limited memory potential, do not stably express IL-10, and are disproportionately lost from the Ag-experienced CD4(+) T cell memory population during the maintenance phase postinfection. CD4(+)YFP(+)GFP(+) T cells generally exhibited a short-lived effector rather than effector memory T cell phenotype postinfection and expressed high levels of PD-1, Lag-3, and TIGIT, indicative of cellular exhaustion. Consistently, the surviving CD4(+)YFP(+)GFP(+) T cell-derived cells were unresponsive and failed to proliferate during the early phase of secondary infection. In contrast, CD4(+)YFP(+)GFP(-) T cell-derived cells expanded rapidly and upregulated IL-10 expression during secondary infection. Correspondingly, CD4(+) T cells were the major producers within an accelerated and amplified IL-10 response during the early stage of secondary malaria infection. Notably, IL-10 exerted quantitatively stronger regulatory effects on innate and CD4(+) T cell responses during primary and secondary infections, respectively. The results in this study significantly improve our understanding of the durability of IL-10-producing CD4(+) T cells postinfection and provide information on how IL-10 may contribute to optimized parasite control and prevention of immune-mediated pathology during repeated malaria infections."}

LitCoin-SeqVar

{"project":"LitCoin-SeqVar","denotations":[{"id":"T1","span":{"begin":610,"end":617},"obj":"SequenceVariant"}],"text":"Long-Lived CD4+IFN-γ+ T Cells rather than Short-Lived CD4+IFN-γ+IL-10+ T Cells Initiate Rapid IL-10 Production To Suppress Anamnestic T Cell Responses during Secondary Malaria Infection.\nCD4(+) T cells that produce IFN-γ are the source of host-protective IL-10 during primary infection with a number of different pathogens, including Plasmodium spp. The fate of these CD4(+)IFN-γ(+)IL-10(+) T cells following clearance of primary infection and their subsequent influence on the course of repeated infections is, however, presently unknown. In this study, utilizing IFN-γ-yellow fluorescent protein (YFP) and IL-10-GFP dual reporter mice, we show that primary malaria infection-induced CD4(+)YFP(+)GFP(+) T cells have limited memory potential, do not stably express IL-10, and are disproportionately lost from the Ag-experienced CD4(+) T cell memory population during the maintenance phase postinfection. CD4(+)YFP(+)GFP(+) T cells generally exhibited a short-lived effector rather than effector memory T cell phenotype postinfection and expressed high levels of PD-1, Lag-3, and TIGIT, indicative of cellular exhaustion. Consistently, the surviving CD4(+)YFP(+)GFP(+) T cell-derived cells were unresponsive and failed to proliferate during the early phase of secondary infection. In contrast, CD4(+)YFP(+)GFP(-) T cell-derived cells expanded rapidly and upregulated IL-10 expression during secondary infection. Correspondingly, CD4(+) T cells were the major producers within an accelerated and amplified IL-10 response during the early stage of secondary malaria infection. Notably, IL-10 exerted quantitatively stronger regulatory effects on innate and CD4(+) T cell responses during primary and secondary infections, respectively. The results in this study significantly improve our understanding of the durability of IL-10-producing CD4(+) T cells postinfection and provide information on how IL-10 may contribute to optimized parasite control and prevention of immune-mediated pathology during repeated malaria infections."}

LitCoin-GeneOrGeneProduct-v0

LitCoin-GeneOrGeneProduct-v2

LitCoin-Disease-MeSH

LitCoin-GeneOrGeneProduct-v3

{"project":"LitCoin-GeneOrGeneProduct-v3","denotations":[{"id":"T1","span":{"begin":0,"end":10},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":15,"end":20},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":58,"end":63},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":64,"end":69},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":94,"end":99},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":215,"end":220},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":255,"end":260},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":374,"end":379},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":382,"end":387},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":565,"end":570},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":571,"end":577},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":608,"end":613},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":765,"end":770},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1062,"end":1066},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1068,"end":1073},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":1079,"end":1084},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":1366,"end":1371},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":1504,"end":1509},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":1583,"end":1588},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":1820,"end":1825},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":1896,"end":1901},"obj":"GeneOrGeneProduct"}],"text":"Long-Lived CD4+IFN-γ+ T Cells rather than Short-Lived CD4+IFN-γ+IL-10+ T Cells Initiate Rapid IL-10 Production To Suppress Anamnestic T Cell Responses during Secondary Malaria Infection.\nCD4(+) T cells that produce IFN-γ are the source of host-protective IL-10 during primary infection with a number of different pathogens, including Plasmodium spp. The fate of these CD4(+)IFN-γ(+)IL-10(+) T cells following clearance of primary infection and their subsequent influence on the course of repeated infections is, however, presently unknown. In this study, utilizing IFN-γ-yellow fluorescent protein (YFP) and IL-10-GFP dual reporter mice, we show that primary malaria infection-induced CD4(+)YFP(+)GFP(+) T cells have limited memory potential, do not stably express IL-10, and are disproportionately lost from the Ag-experienced CD4(+) T cell memory population during the maintenance phase postinfection. CD4(+)YFP(+)GFP(+) T cells generally exhibited a short-lived effector rather than effector memory T cell phenotype postinfection and expressed high levels of PD-1, Lag-3, and TIGIT, indicative of cellular exhaustion. Consistently, the surviving CD4(+)YFP(+)GFP(+) T cell-derived cells were unresponsive and failed to proliferate during the early phase of secondary infection. In contrast, CD4(+)YFP(+)GFP(-) T cell-derived cells expanded rapidly and upregulated IL-10 expression during secondary infection. Correspondingly, CD4(+) T cells were the major producers within an accelerated and amplified IL-10 response during the early stage of secondary malaria infection. Notably, IL-10 exerted quantitatively stronger regulatory effects on innate and CD4(+) T cell responses during primary and secondary infections, respectively. The results in this study significantly improve our understanding of the durability of IL-10-producing CD4(+) T cells postinfection and provide information on how IL-10 may contribute to optimized parasite control and prevention of immune-mediated pathology during repeated malaria infections."}

LitCoin_Mondo_095

{"project":"LitCoin_Mondo_095","denotations":[{"id":"T1","span":{"begin":168,"end":175},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":176,"end":185},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":276,"end":285},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":430,"end":439},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":659,"end":666},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":667,"end":676},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1062,"end":1064},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":1269,"end":1278},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":1400,"end":1409},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":1555,"end":1562},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":1563,"end":1572},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":2007,"end":2014},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005136"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005550"},{"id":"A12","pred":"mondo_id","subj":"T12","obj":"0005550"},{"id":"A11","pred":"mondo_id","subj":"T11","obj":"0005136"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0005550"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"0015873"},{"id":"A8","pred":"mondo_id","subj":"T7","obj":"0008199"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0005550"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005550"},{"id":"A10","pred":"mondo_id","subj":"T10","obj":"0005550"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0005136"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"0005550"},{"id":"A13","pred":"mondo_id","subj":"T13","obj":"0005136"}],"text":"Long-Lived CD4+IFN-γ+ T Cells rather than Short-Lived CD4+IFN-γ+IL-10+ T Cells Initiate Rapid IL-10 Production To Suppress Anamnestic T Cell Responses during Secondary Malaria Infection.\nCD4(+) T cells that produce IFN-γ are the source of host-protective IL-10 during primary infection with a number of different pathogens, including Plasmodium spp. The fate of these CD4(+)IFN-γ(+)IL-10(+) T cells following clearance of primary infection and their subsequent influence on the course of repeated infections is, however, presently unknown. In this study, utilizing IFN-γ-yellow fluorescent protein (YFP) and IL-10-GFP dual reporter mice, we show that primary malaria infection-induced CD4(+)YFP(+)GFP(+) T cells have limited memory potential, do not stably express IL-10, and are disproportionately lost from the Ag-experienced CD4(+) T cell memory population during the maintenance phase postinfection. CD4(+)YFP(+)GFP(+) T cells generally exhibited a short-lived effector rather than effector memory T cell phenotype postinfection and expressed high levels of PD-1, Lag-3, and TIGIT, indicative of cellular exhaustion. Consistently, the surviving CD4(+)YFP(+)GFP(+) T cell-derived cells were unresponsive and failed to proliferate during the early phase of secondary infection. In contrast, CD4(+)YFP(+)GFP(-) T cell-derived cells expanded rapidly and upregulated IL-10 expression during secondary infection. Correspondingly, CD4(+) T cells were the major producers within an accelerated and amplified IL-10 response during the early stage of secondary malaria infection. Notably, IL-10 exerted quantitatively stronger regulatory effects on innate and CD4(+) T cell responses during primary and secondary infections, respectively. The results in this study significantly improve our understanding of the durability of IL-10-producing CD4(+) T cells postinfection and provide information on how IL-10 may contribute to optimized parasite control and prevention of immune-mediated pathology during repeated malaria infections."}

LitCoin-MeSH-Disease-2

{"project":"LitCoin-MeSH-Disease-2","denotations":[{"id":"T1","span":{"begin":168,"end":175},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":176,"end":185},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":276,"end":285},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":430,"end":439},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":497,"end":507},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":659,"end":666},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":667,"end":676},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1259,"end":1278},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":1390,"end":1409},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":1555,"end":1562},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":1563,"end":1572},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":1697,"end":1717},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":2007,"end":2014},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":2015,"end":2025},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A14","pred":"ID:","subj":"T14","obj":"D007239"},{"id":"A10","pred":"ID:","subj":"T10","obj":"D008288"},{"id":"A13","pred":"ID:","subj":"T13","obj":"D008288"},{"id":"A3","pred":"ID:","subj":"T3","obj":"D007239"},{"id":"A2","pred":"ID:","subj":"T2","obj":"D007239"},{"id":"A5","pred":"ID:","subj":"T5","obj":"D007239"},{"id":"A12","pred":"ID:","subj":"T12","obj":"D060085"},{"id":"A4","pred":"ID:","subj":"T4","obj":"D007239"},{"id":"A11","pred":"ID:","subj":"T11","obj":"D007239"},{"id":"A6","pred":"ID:","subj":"T6","obj":"D008288"},{"id":"A8","pred":"ID:","subj":"T8","obj":"D060085"},{"id":"A9","pred":"ID:","subj":"T9","obj":"D060085"},{"id":"A1","pred":"ID:","subj":"T1","obj":"D008288"},{"id":"A7","pred":"ID:","subj":"T7","obj":"D007239"}],"text":"Long-Lived CD4+IFN-γ+ T Cells rather than Short-Lived CD4+IFN-γ+IL-10+ T Cells Initiate Rapid IL-10 Production To Suppress Anamnestic T Cell Responses during Secondary Malaria Infection.\nCD4(+) T cells that produce IFN-γ are the source of host-protective IL-10 during primary infection with a number of different pathogens, including Plasmodium spp. The fate of these CD4(+)IFN-γ(+)IL-10(+) T cells following clearance of primary infection and their subsequent influence on the course of repeated infections is, however, presently unknown. In this study, utilizing IFN-γ-yellow fluorescent protein (YFP) and IL-10-GFP dual reporter mice, we show that primary malaria infection-induced CD4(+)YFP(+)GFP(+) T cells have limited memory potential, do not stably express IL-10, and are disproportionately lost from the Ag-experienced CD4(+) T cell memory population during the maintenance phase postinfection. CD4(+)YFP(+)GFP(+) T cells generally exhibited a short-lived effector rather than effector memory T cell phenotype postinfection and expressed high levels of PD-1, Lag-3, and TIGIT, indicative of cellular exhaustion. Consistently, the surviving CD4(+)YFP(+)GFP(+) T cell-derived cells were unresponsive and failed to proliferate during the early phase of secondary infection. In contrast, CD4(+)YFP(+)GFP(-) T cell-derived cells expanded rapidly and upregulated IL-10 expression during secondary infection. Correspondingly, CD4(+) T cells were the major producers within an accelerated and amplified IL-10 response during the early stage of secondary malaria infection. Notably, IL-10 exerted quantitatively stronger regulatory effects on innate and CD4(+) T cell responses during primary and secondary infections, respectively. The results in this study significantly improve our understanding of the durability of IL-10-producing CD4(+) T cells postinfection and provide information on how IL-10 may contribute to optimized parasite control and prevention of immune-mediated pathology during repeated malaria infections."}

LitCoin-MONDO_bioort2019

{"project":"LitCoin-MONDO_bioort2019","denotations":[{"id":"T1","span":{"begin":168,"end":175},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":659,"end":666},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":1259,"end":1278},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":1390,"end":1409},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":1555,"end":1562},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1697,"end":1717},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":2007,"end":2014},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"#label","subj":"T1","obj":"D008288"},{"id":"A2","pred":"#label","subj":"T2","obj":"D008288"},{"id":"A3","pred":"#label","subj":"T3","obj":"D060085"},{"id":"A4","pred":"#label","subj":"T4","obj":"D060085"},{"id":"A5","pred":"#label","subj":"T5","obj":"D008288"},{"id":"A6","pred":"#label","subj":"T6","obj":"D060085"},{"id":"A7","pred":"#label","subj":"T7","obj":"D008288"}],"text":"Long-Lived CD4+IFN-γ+ T Cells rather than Short-Lived CD4+IFN-γ+IL-10+ T Cells Initiate Rapid IL-10 Production To Suppress Anamnestic T Cell Responses during Secondary Malaria Infection.\nCD4(+) T cells that produce IFN-γ are the source of host-protective IL-10 during primary infection with a number of different pathogens, including Plasmodium spp. The fate of these CD4(+)IFN-γ(+)IL-10(+) T cells following clearance of primary infection and their subsequent influence on the course of repeated infections is, however, presently unknown. In this study, utilizing IFN-γ-yellow fluorescent protein (YFP) and IL-10-GFP dual reporter mice, we show that primary malaria infection-induced CD4(+)YFP(+)GFP(+) T cells have limited memory potential, do not stably express IL-10, and are disproportionately lost from the Ag-experienced CD4(+) T cell memory population during the maintenance phase postinfection. CD4(+)YFP(+)GFP(+) T cells generally exhibited a short-lived effector rather than effector memory T cell phenotype postinfection and expressed high levels of PD-1, Lag-3, and TIGIT, indicative of cellular exhaustion. Consistently, the surviving CD4(+)YFP(+)GFP(+) T cell-derived cells were unresponsive and failed to proliferate during the early phase of secondary infection. In contrast, CD4(+)YFP(+)GFP(-) T cell-derived cells expanded rapidly and upregulated IL-10 expression during secondary infection. Correspondingly, CD4(+) T cells were the major producers within an accelerated and amplified IL-10 response during the early stage of secondary malaria infection. Notably, IL-10 exerted quantitatively stronger regulatory effects on innate and CD4(+) T cell responses during primary and secondary infections, respectively. The results in this study significantly improve our understanding of the durability of IL-10-producing CD4(+) T cells postinfection and provide information on how IL-10 may contribute to optimized parasite control and prevention of immune-mediated pathology during repeated malaria infections."}

LitCoin-NCBITaxon-2

{"project":"LitCoin-NCBITaxon-2","denotations":[{"id":"T1","span":{"begin":334,"end":344},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":632,"end":636},"obj":"OrganismTaxon"}],"text":"Long-Lived CD4+IFN-γ+ T Cells rather than Short-Lived CD4+IFN-γ+IL-10+ T Cells Initiate Rapid IL-10 Production To Suppress Anamnestic T Cell Responses during Secondary Malaria Infection.\nCD4(+) T cells that produce IFN-γ are the source of host-protective IL-10 during primary infection with a number of different pathogens, including Plasmodium spp. The fate of these CD4(+)IFN-γ(+)IL-10(+) T cells following clearance of primary infection and their subsequent influence on the course of repeated infections is, however, presently unknown. In this study, utilizing IFN-γ-yellow fluorescent protein (YFP) and IL-10-GFP dual reporter mice, we show that primary malaria infection-induced CD4(+)YFP(+)GFP(+) T cells have limited memory potential, do not stably express IL-10, and are disproportionately lost from the Ag-experienced CD4(+) T cell memory population during the maintenance phase postinfection. CD4(+)YFP(+)GFP(+) T cells generally exhibited a short-lived effector rather than effector memory T cell phenotype postinfection and expressed high levels of PD-1, Lag-3, and TIGIT, indicative of cellular exhaustion. Consistently, the surviving CD4(+)YFP(+)GFP(+) T cell-derived cells were unresponsive and failed to proliferate during the early phase of secondary infection. In contrast, CD4(+)YFP(+)GFP(-) T cell-derived cells expanded rapidly and upregulated IL-10 expression during secondary infection. Correspondingly, CD4(+) T cells were the major producers within an accelerated and amplified IL-10 response during the early stage of secondary malaria infection. Notably, IL-10 exerted quantitatively stronger regulatory effects on innate and CD4(+) T cell responses during primary and secondary infections, respectively. The results in this study significantly improve our understanding of the durability of IL-10-producing CD4(+) T cells postinfection and provide information on how IL-10 may contribute to optimized parasite control and prevention of immune-mediated pathology during repeated malaria infections."}

LitCoin-training-merged