PubMed:31110314
Annnotations
PubMed_ArguminSci
{"project":"PubMed_ArguminSci","denotations":[{"id":"T1","span":{"begin":71,"end":180},"obj":"DRI_Challenge"},{"id":"T2","span":{"begin":181,"end":306},"obj":"DRI_Background"},{"id":"T3","span":{"begin":307,"end":463},"obj":"DRI_Challenge"},{"id":"T4","span":{"begin":464,"end":537},"obj":"DRI_Background"},{"id":"T5","span":{"begin":538,"end":546},"obj":"DRI_Background"},{"id":"T6","span":{"begin":567,"end":678},"obj":"DRI_Background"},{"id":"T7","span":{"begin":679,"end":856},"obj":"DRI_Approach"},{"id":"T8","span":{"begin":857,"end":998},"obj":"DRI_Outcome"}],"text":"CD8+ T cells induce cachexia during chronic viral infection.\nCachexia represents a leading cause of morbidity and mortality in various cancers, chronic inflammation and infections. Understanding of the mechanisms that drive cachexia has remained limited, especially for infection-associated cachexia (IAC). In the present paper we describe a model of reversible cachexia in mice with chronic viral infection and identify an essential role for CD8+ T cells in IAC. Cytokines linked to cancer-associated cachexia did not contribute to IAC. Instead, virus-specific CD8+ T cells caused morphologic and molecular changes in the adipose tissue, which led to depletion of lipid stores. These changes occurred at a time point that preceded the peak of the CD8+ T cell response and required T cell-intrinsic type I interferon signaling and antigen-specific priming. Our results link systemic antiviral immune responses to adipose-tissue remodeling and reveal an underappreciated role of CD8+ T cells in IAC."}
Goldhamster2_Cellosaurus
{"project":"Goldhamster2_Cellosaurus","denotations":[{"id":"T1","span":{"begin":81,"end":82},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T2","span":{"begin":135,"end":142},"obj":"CVCL_E025|Induced_pluripotent_stem_cell|Homo sapiens"},{"id":"T3","span":{"begin":233,"end":236},"obj":"CVCL_6758|Undefined_cell_line_type|Cricetulus griseus"},{"id":"T4","span":{"begin":233,"end":236},"obj":"CVCL_E689|Transformed_cell_line|Homo sapiens"},{"id":"T5","span":{"begin":301,"end":304},"obj":"CVCL_X373|Transformed_cell_line|Rattus norvegicus"},{"id":"T6","span":{"begin":328,"end":330},"obj":"CVCL_5M23|Cancer_cell_line|Mesocricetus auratus"},{"id":"T7","span":{"begin":340,"end":341},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T8","span":{"begin":421,"end":423},"obj":"CVCL_8754|Cancer_cell_line|Homo sapiens"},{"id":"T9","span":{"begin":421,"end":423},"obj":"CVCL_H241|Cancer_cell_line|Homo sapiens"},{"id":"T10","span":{"begin":459,"end":462},"obj":"CVCL_X373|Transformed_cell_line|Rattus norvegicus"},{"id":"T11","span":{"begin":484,"end":490},"obj":"CVCL_E025|Induced_pluripotent_stem_cell|Homo sapiens"},{"id":"T12","span":{"begin":533,"end":536},"obj":"CVCL_X373|Transformed_cell_line|Rattus norvegicus"},{"id":"T13","span":{"begin":608,"end":615},"obj":"CVCL_0238|Cancer_cell_line|Homo sapiens"},{"id":"T14","span":{"begin":685,"end":692},"obj":"CVCL_0238|Cancer_cell_line|Homo sapiens"},{"id":"T15","span":{"begin":705,"end":706},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T16","span":{"begin":707,"end":711},"obj":"CVCL_0047|Telomerase_immortalized_cell_line|Homo sapiens"},{"id":"T17","span":{"begin":736,"end":740},"obj":"CVCL_3772|Transformed_cell_line|Homo sapiens"},{"id":"T18","span":{"begin":950,"end":952},"obj":"CVCL_8754|Cancer_cell_line|Homo sapiens"},{"id":"T19","span":{"begin":950,"end":952},"obj":"CVCL_H241|Cancer_cell_line|Homo sapiens"},{"id":"T20","span":{"begin":994,"end":997},"obj":"CVCL_X373|Transformed_cell_line|Rattus norvegicus"}],"text":"CD8+ T cells induce cachexia during chronic viral infection.\nCachexia represents a leading cause of morbidity and mortality in various cancers, chronic inflammation and infections. Understanding of the mechanisms that drive cachexia has remained limited, especially for infection-associated cachexia (IAC). In the present paper we describe a model of reversible cachexia in mice with chronic viral infection and identify an essential role for CD8+ T cells in IAC. Cytokines linked to cancer-associated cachexia did not contribute to IAC. Instead, virus-specific CD8+ T cells caused morphologic and molecular changes in the adipose tissue, which led to depletion of lipid stores. These changes occurred at a time point that preceded the peak of the CD8+ T cell response and required T cell-intrinsic type I interferon signaling and antigen-specific priming. Our results link systemic antiviral immune responses to adipose-tissue remodeling and reveal an underappreciated role of CD8+ T cells in IAC."}
Inflammaging
{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":60},"obj":"Sentence"},{"id":"T2","span":{"begin":61,"end":180},"obj":"Sentence"},{"id":"T3","span":{"begin":181,"end":306},"obj":"Sentence"},{"id":"T4","span":{"begin":307,"end":463},"obj":"Sentence"},{"id":"T5","span":{"begin":464,"end":537},"obj":"Sentence"},{"id":"T6","span":{"begin":538,"end":678},"obj":"Sentence"},{"id":"T7","span":{"begin":679,"end":856},"obj":"Sentence"},{"id":"T8","span":{"begin":857,"end":998},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":60},"obj":"Sentence"},{"id":"T2","span":{"begin":61,"end":180},"obj":"Sentence"},{"id":"T3","span":{"begin":181,"end":306},"obj":"Sentence"},{"id":"T4","span":{"begin":307,"end":463},"obj":"Sentence"},{"id":"T5","span":{"begin":464,"end":537},"obj":"Sentence"},{"id":"T6","span":{"begin":538,"end":678},"obj":"Sentence"},{"id":"T7","span":{"begin":679,"end":856},"obj":"Sentence"},{"id":"T8","span":{"begin":857,"end":998},"obj":"Sentence"}],"text":"CD8+ T cells induce cachexia during chronic viral infection.\nCachexia represents a leading cause of morbidity and mortality in various cancers, chronic inflammation and infections. Understanding of the mechanisms that drive cachexia has remained limited, especially for infection-associated cachexia (IAC). In the present paper we describe a model of reversible cachexia in mice with chronic viral infection and identify an essential role for CD8+ T cells in IAC. Cytokines linked to cancer-associated cachexia did not contribute to IAC. Instead, virus-specific CD8+ T cells caused morphologic and molecular changes in the adipose tissue, which led to depletion of lipid stores. These changes occurred at a time point that preceded the peak of the CD8+ T cell response and required T cell-intrinsic type I interferon signaling and antigen-specific priming. Our results link systemic antiviral immune responses to adipose-tissue remodeling and reveal an underappreciated role of CD8+ T cells in IAC."}
GoldHamster
{"project":"GoldHamster","denotations":[{"id":"T1","span":{"begin":20,"end":28},"obj":"D002100"},{"id":"T2","span":{"begin":20,"end":28},"obj":"D002100"},{"id":"T3","span":{"begin":44,"end":59},"obj":"GO:0016032"},{"id":"T4","span":{"begin":44,"end":59},"obj":"D014777"},{"id":"T5","span":{"begin":44,"end":59},"obj":"D014777"},{"id":"T8","span":{"begin":135,"end":142},"obj":"D009369"},{"id":"T9","span":{"begin":135,"end":142},"obj":"D009369"},{"id":"T10","span":{"begin":152,"end":164},"obj":"GO:0006954"},{"id":"T11","span":{"begin":152,"end":164},"obj":"D007249"},{"id":"T12","span":{"begin":152,"end":164},"obj":"D007249"},{"id":"T13","span":{"begin":224,"end":232},"obj":"D002100"},{"id":"T14","span":{"begin":224,"end":232},"obj":"D002100"},{"id":"T15","span":{"begin":270,"end":279},"obj":"D007239"},{"id":"T16","span":{"begin":270,"end":279},"obj":"D007239"},{"id":"T17","span":{"begin":291,"end":299},"obj":"D002100"},{"id":"T18","span":{"begin":291,"end":299},"obj":"D002100"},{"id":"T20","span":{"begin":301,"end":304},"obj":"CVCL_X373"},{"id":"T19","span":{"begin":301,"end":304},"obj":"UBERON:2002269"},{"id":"T21","span":{"begin":362,"end":370},"obj":"D002100"},{"id":"T22","span":{"begin":362,"end":370},"obj":"D002100"},{"id":"T23","span":{"begin":374,"end":378},"obj":"PR:000005054"},{"id":"T25","span":{"begin":374,"end":378},"obj":"O89094"},{"id":"T24","span":{"begin":374,"end":378},"obj":"D051379"},{"id":"T26","span":{"begin":374,"end":378},"obj":"10095"},{"id":"T27","span":{"begin":392,"end":407},"obj":"GO:0016032"},{"id":"T28","span":{"begin":392,"end":407},"obj":"D014777"},{"id":"T29","span":{"begin":392,"end":407},"obj":"D014777"},{"id":"T33","span":{"begin":459,"end":462},"obj":"CVCL_X373"},{"id":"T32","span":{"begin":459,"end":462},"obj":"UBERON:2002269"},{"id":"T34","span":{"begin":464,"end":473},"obj":"D016207"},{"id":"T35","span":{"begin":464,"end":473},"obj":"D016207"},{"id":"T36","span":{"begin":502,"end":510},"obj":"D002100"},{"id":"T37","span":{"begin":502,"end":510},"obj":"D002100"},{"id":"T39","span":{"begin":533,"end":536},"obj":"CVCL_X373"},{"id":"T38","span":{"begin":533,"end":536},"obj":"UBERON:2002269"},{"id":"T41","span":{"begin":623,"end":637},"obj":"UBERON:0001013"},{"id":"T43","span":{"begin":665,"end":670},"obj":"CHEBI:18059"},{"id":"T44","span":{"begin":753,"end":759},"obj":"CL:0000084"},{"id":"T45","span":{"begin":782,"end":788},"obj":"CL:0000084"},{"id":"T48","span":{"begin":799,"end":816},"obj":"PR:000025848"},{"id":"T46","span":{"begin":799,"end":816},"obj":"D007370"},{"id":"T47","span":{"begin":799,"end":816},"obj":"D007370"},{"id":"T54","span":{"begin":817,"end":826},"obj":"GO:0023052"},{"id":"T55","span":{"begin":831,"end":838},"obj":"D000941"},{"id":"T56","span":{"begin":831,"end":838},"obj":"CHEBI:59132"},{"id":"T57","span":{"begin":831,"end":838},"obj":"D000941"},{"id":"T58","span":{"begin":883,"end":892},"obj":"CHEBI:22587"},{"id":"T60","span":{"begin":913,"end":927},"obj":"UBERON:0001013"},{"id":"T62","span":{"begin":921,"end":938},"obj":"GO:0048771"},{"id":"T64","span":{"begin":994,"end":997},"obj":"CVCL_X373"},{"id":"T63","span":{"begin":994,"end":997},"obj":"UBERON:2002269"}],"text":"CD8+ T cells induce cachexia during chronic viral infection.\nCachexia represents a leading cause of morbidity and mortality in various cancers, chronic inflammation and infections. Understanding of the mechanisms that drive cachexia has remained limited, especially for infection-associated cachexia (IAC). In the present paper we describe a model of reversible cachexia in mice with chronic viral infection and identify an essential role for CD8+ T cells in IAC. Cytokines linked to cancer-associated cachexia did not contribute to IAC. Instead, virus-specific CD8+ T cells caused morphologic and molecular changes in the adipose tissue, which led to depletion of lipid stores. These changes occurred at a time point that preceded the peak of the CD8+ T cell response and required T cell-intrinsic type I interferon signaling and antigen-specific priming. Our results link systemic antiviral immune responses to adipose-tissue remodeling and reveal an underappreciated role of CD8+ T cells in IAC."}