Single‐cell immune profiling reveals markers of emergency myelopoiesis that distinguish severe from mild respiratory syncytial virus disease in infants
Abstract Whereas most infants infected with respiratory syncytial virus (RSV) show no or only mild symptoms, an estimated 3 million children under five are hospitalized annually due to RSV disease. This study aimed to investigate biological mechanisms and associated biomarkers underlying RSV disease...
Ausführliche Beschreibung
Autor*in: |
Nevena Zivanovic [verfasserIn] Deniz Öner [verfasserIn] Yann Abraham [verfasserIn] Joseph McGinley [verfasserIn] Simon B. Drysdale [verfasserIn] Joanne G. Wildenbeest [verfasserIn] Marjolein Crabbe [verfasserIn] Greet Vanhoof [verfasserIn] Kim Thys [verfasserIn] Ryan S. Thwaites [verfasserIn] Hannah Robinson [verfasserIn] Louis Bont [verfasserIn] Peter J. M. Openshaw [verfasserIn] Federico Martinón‐Torres [verfasserIn] RESCEU Investigators [verfasserIn] Andrew J. Pollard [verfasserIn] Jeroen Aerssens [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2023 |
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Übergeordnetes Werk: |
In: Clinical and Translational Medicine - Wiley, 2013, 13(2023), 12, Seite n/a-n/a |
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Übergeordnetes Werk: |
volume:13 ; year:2023 ; number:12 ; pages:n/a-n/a |
Links: |
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DOI / URN: |
10.1002/ctm2.1507 |
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Katalog-ID: |
DOAJ098089560 |
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520 | |a Abstract Whereas most infants infected with respiratory syncytial virus (RSV) show no or only mild symptoms, an estimated 3 million children under five are hospitalized annually due to RSV disease. This study aimed to investigate biological mechanisms and associated biomarkers underlying RSV disease heterogeneity in young infants, enabling the potential to objectively categorize RSV‐infected infants according to their medical needs. Immunophenotypic and functional profiling demonstrated the emergence of immature and progenitor‐like neutrophils, proliferative monocytes (HLA‐DRLow, Ki67+), impaired antigen‐presenting function, downregulation of T cell response and low abundance of HLA‐DRLow B cells in severe RSV disease. HLA‐DRLow monocytes were found as a hallmark of RSV‐infected infants requiring hospitalization. Complementary transcriptomics identified genes associated with disease severity and pointed to the emergency myelopoiesis response. These results shed new light on mechanisms underlying the pathogenesis and development of severe RSV disease and identified potential new candidate biomarkers for patient stratification. | ||
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700 | 0 | |a Yann Abraham |e verfasserin |4 aut | |
700 | 0 | |a Joseph McGinley |e verfasserin |4 aut | |
700 | 0 | |a Simon B. Drysdale |e verfasserin |4 aut | |
700 | 0 | |a Joanne G. Wildenbeest |e verfasserin |4 aut | |
700 | 0 | |a Marjolein Crabbe |e verfasserin |4 aut | |
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700 | 0 | |a Federico Martinón‐Torres |e verfasserin |4 aut | |
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10.1002/ctm2.1507 doi (DE-627)DOAJ098089560 (DE-599)DOAJac35e4f76db64145b22518aa1ef50b98 DE-627 ger DE-627 rakwb eng R5-920 Nevena Zivanovic verfasserin aut Single‐cell immune profiling reveals markers of emergency myelopoiesis that distinguish severe from mild respiratory syncytial virus disease in infants 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Whereas most infants infected with respiratory syncytial virus (RSV) show no or only mild symptoms, an estimated 3 million children under five are hospitalized annually due to RSV disease. This study aimed to investigate biological mechanisms and associated biomarkers underlying RSV disease heterogeneity in young infants, enabling the potential to objectively categorize RSV‐infected infants according to their medical needs. Immunophenotypic and functional profiling demonstrated the emergence of immature and progenitor‐like neutrophils, proliferative monocytes (HLA‐DRLow, Ki67+), impaired antigen‐presenting function, downregulation of T cell response and low abundance of HLA‐DRLow B cells in severe RSV disease. HLA‐DRLow monocytes were found as a hallmark of RSV‐infected infants requiring hospitalization. Complementary transcriptomics identified genes associated with disease severity and pointed to the emergency myelopoiesis response. These results shed new light on mechanisms underlying the pathogenesis and development of severe RSV disease and identified potential new candidate biomarkers for patient stratification. Medicine (General) Deniz Öner verfasserin aut Yann Abraham verfasserin aut Joseph McGinley verfasserin aut Simon B. Drysdale verfasserin aut Joanne G. Wildenbeest verfasserin aut Marjolein Crabbe verfasserin aut Greet Vanhoof verfasserin aut Kim Thys verfasserin aut Ryan S. Thwaites verfasserin aut Hannah Robinson verfasserin aut Louis Bont verfasserin aut Peter J. M. Openshaw verfasserin aut Federico Martinón‐Torres verfasserin aut RESCEU Investigators verfasserin aut Andrew J. Pollard verfasserin aut Jeroen Aerssens verfasserin aut In Clinical and Translational Medicine Wiley, 2013 13(2023), 12, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:13 year:2023 number:12 pages:n/a-n/a https://doi.org/10.1002/ctm2.1507 kostenfrei https://doaj.org/article/ac35e4f76db64145b22518aa1ef50b98 kostenfrei https://doi.org/10.1002/ctm2.1507 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2023 12 n/a-n/a |
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10.1002/ctm2.1507 doi (DE-627)DOAJ098089560 (DE-599)DOAJac35e4f76db64145b22518aa1ef50b98 DE-627 ger DE-627 rakwb eng R5-920 Nevena Zivanovic verfasserin aut Single‐cell immune profiling reveals markers of emergency myelopoiesis that distinguish severe from mild respiratory syncytial virus disease in infants 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Whereas most infants infected with respiratory syncytial virus (RSV) show no or only mild symptoms, an estimated 3 million children under five are hospitalized annually due to RSV disease. This study aimed to investigate biological mechanisms and associated biomarkers underlying RSV disease heterogeneity in young infants, enabling the potential to objectively categorize RSV‐infected infants according to their medical needs. Immunophenotypic and functional profiling demonstrated the emergence of immature and progenitor‐like neutrophils, proliferative monocytes (HLA‐DRLow, Ki67+), impaired antigen‐presenting function, downregulation of T cell response and low abundance of HLA‐DRLow B cells in severe RSV disease. HLA‐DRLow monocytes were found as a hallmark of RSV‐infected infants requiring hospitalization. Complementary transcriptomics identified genes associated with disease severity and pointed to the emergency myelopoiesis response. These results shed new light on mechanisms underlying the pathogenesis and development of severe RSV disease and identified potential new candidate biomarkers for patient stratification. Medicine (General) Deniz Öner verfasserin aut Yann Abraham verfasserin aut Joseph McGinley verfasserin aut Simon B. Drysdale verfasserin aut Joanne G. Wildenbeest verfasserin aut Marjolein Crabbe verfasserin aut Greet Vanhoof verfasserin aut Kim Thys verfasserin aut Ryan S. Thwaites verfasserin aut Hannah Robinson verfasserin aut Louis Bont verfasserin aut Peter J. M. Openshaw verfasserin aut Federico Martinón‐Torres verfasserin aut RESCEU Investigators verfasserin aut Andrew J. Pollard verfasserin aut Jeroen Aerssens verfasserin aut In Clinical and Translational Medicine Wiley, 2013 13(2023), 12, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:13 year:2023 number:12 pages:n/a-n/a https://doi.org/10.1002/ctm2.1507 kostenfrei https://doaj.org/article/ac35e4f76db64145b22518aa1ef50b98 kostenfrei https://doi.org/10.1002/ctm2.1507 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2023 12 n/a-n/a |
allfields_unstemmed |
10.1002/ctm2.1507 doi (DE-627)DOAJ098089560 (DE-599)DOAJac35e4f76db64145b22518aa1ef50b98 DE-627 ger DE-627 rakwb eng R5-920 Nevena Zivanovic verfasserin aut Single‐cell immune profiling reveals markers of emergency myelopoiesis that distinguish severe from mild respiratory syncytial virus disease in infants 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Whereas most infants infected with respiratory syncytial virus (RSV) show no or only mild symptoms, an estimated 3 million children under five are hospitalized annually due to RSV disease. This study aimed to investigate biological mechanisms and associated biomarkers underlying RSV disease heterogeneity in young infants, enabling the potential to objectively categorize RSV‐infected infants according to their medical needs. Immunophenotypic and functional profiling demonstrated the emergence of immature and progenitor‐like neutrophils, proliferative monocytes (HLA‐DRLow, Ki67+), impaired antigen‐presenting function, downregulation of T cell response and low abundance of HLA‐DRLow B cells in severe RSV disease. HLA‐DRLow monocytes were found as a hallmark of RSV‐infected infants requiring hospitalization. Complementary transcriptomics identified genes associated with disease severity and pointed to the emergency myelopoiesis response. These results shed new light on mechanisms underlying the pathogenesis and development of severe RSV disease and identified potential new candidate biomarkers for patient stratification. Medicine (General) Deniz Öner verfasserin aut Yann Abraham verfasserin aut Joseph McGinley verfasserin aut Simon B. Drysdale verfasserin aut Joanne G. Wildenbeest verfasserin aut Marjolein Crabbe verfasserin aut Greet Vanhoof verfasserin aut Kim Thys verfasserin aut Ryan S. Thwaites verfasserin aut Hannah Robinson verfasserin aut Louis Bont verfasserin aut Peter J. M. Openshaw verfasserin aut Federico Martinón‐Torres verfasserin aut RESCEU Investigators verfasserin aut Andrew J. Pollard verfasserin aut Jeroen Aerssens verfasserin aut In Clinical and Translational Medicine Wiley, 2013 13(2023), 12, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:13 year:2023 number:12 pages:n/a-n/a https://doi.org/10.1002/ctm2.1507 kostenfrei https://doaj.org/article/ac35e4f76db64145b22518aa1ef50b98 kostenfrei https://doi.org/10.1002/ctm2.1507 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2023 12 n/a-n/a |
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10.1002/ctm2.1507 doi (DE-627)DOAJ098089560 (DE-599)DOAJac35e4f76db64145b22518aa1ef50b98 DE-627 ger DE-627 rakwb eng R5-920 Nevena Zivanovic verfasserin aut Single‐cell immune profiling reveals markers of emergency myelopoiesis that distinguish severe from mild respiratory syncytial virus disease in infants 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Whereas most infants infected with respiratory syncytial virus (RSV) show no or only mild symptoms, an estimated 3 million children under five are hospitalized annually due to RSV disease. This study aimed to investigate biological mechanisms and associated biomarkers underlying RSV disease heterogeneity in young infants, enabling the potential to objectively categorize RSV‐infected infants according to their medical needs. Immunophenotypic and functional profiling demonstrated the emergence of immature and progenitor‐like neutrophils, proliferative monocytes (HLA‐DRLow, Ki67+), impaired antigen‐presenting function, downregulation of T cell response and low abundance of HLA‐DRLow B cells in severe RSV disease. HLA‐DRLow monocytes were found as a hallmark of RSV‐infected infants requiring hospitalization. Complementary transcriptomics identified genes associated with disease severity and pointed to the emergency myelopoiesis response. These results shed new light on mechanisms underlying the pathogenesis and development of severe RSV disease and identified potential new candidate biomarkers for patient stratification. Medicine (General) Deniz Öner verfasserin aut Yann Abraham verfasserin aut Joseph McGinley verfasserin aut Simon B. Drysdale verfasserin aut Joanne G. Wildenbeest verfasserin aut Marjolein Crabbe verfasserin aut Greet Vanhoof verfasserin aut Kim Thys verfasserin aut Ryan S. Thwaites verfasserin aut Hannah Robinson verfasserin aut Louis Bont verfasserin aut Peter J. M. Openshaw verfasserin aut Federico Martinón‐Torres verfasserin aut RESCEU Investigators verfasserin aut Andrew J. Pollard verfasserin aut Jeroen Aerssens verfasserin aut In Clinical and Translational Medicine Wiley, 2013 13(2023), 12, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:13 year:2023 number:12 pages:n/a-n/a https://doi.org/10.1002/ctm2.1507 kostenfrei https://doaj.org/article/ac35e4f76db64145b22518aa1ef50b98 kostenfrei https://doi.org/10.1002/ctm2.1507 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2023 12 n/a-n/a |
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10.1002/ctm2.1507 doi (DE-627)DOAJ098089560 (DE-599)DOAJac35e4f76db64145b22518aa1ef50b98 DE-627 ger DE-627 rakwb eng R5-920 Nevena Zivanovic verfasserin aut Single‐cell immune profiling reveals markers of emergency myelopoiesis that distinguish severe from mild respiratory syncytial virus disease in infants 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Whereas most infants infected with respiratory syncytial virus (RSV) show no or only mild symptoms, an estimated 3 million children under five are hospitalized annually due to RSV disease. This study aimed to investigate biological mechanisms and associated biomarkers underlying RSV disease heterogeneity in young infants, enabling the potential to objectively categorize RSV‐infected infants according to their medical needs. Immunophenotypic and functional profiling demonstrated the emergence of immature and progenitor‐like neutrophils, proliferative monocytes (HLA‐DRLow, Ki67+), impaired antigen‐presenting function, downregulation of T cell response and low abundance of HLA‐DRLow B cells in severe RSV disease. HLA‐DRLow monocytes were found as a hallmark of RSV‐infected infants requiring hospitalization. Complementary transcriptomics identified genes associated with disease severity and pointed to the emergency myelopoiesis response. These results shed new light on mechanisms underlying the pathogenesis and development of severe RSV disease and identified potential new candidate biomarkers for patient stratification. Medicine (General) Deniz Öner verfasserin aut Yann Abraham verfasserin aut Joseph McGinley verfasserin aut Simon B. Drysdale verfasserin aut Joanne G. Wildenbeest verfasserin aut Marjolein Crabbe verfasserin aut Greet Vanhoof verfasserin aut Kim Thys verfasserin aut Ryan S. Thwaites verfasserin aut Hannah Robinson verfasserin aut Louis Bont verfasserin aut Peter J. M. Openshaw verfasserin aut Federico Martinón‐Torres verfasserin aut RESCEU Investigators verfasserin aut Andrew J. Pollard verfasserin aut Jeroen Aerssens verfasserin aut In Clinical and Translational Medicine Wiley, 2013 13(2023), 12, Seite n/a-n/a (DE-627)733752837 (DE-600)2697013-2 20011326 nnns volume:13 year:2023 number:12 pages:n/a-n/a https://doi.org/10.1002/ctm2.1507 kostenfrei https://doaj.org/article/ac35e4f76db64145b22518aa1ef50b98 kostenfrei https://doi.org/10.1002/ctm2.1507 kostenfrei https://doaj.org/toc/2001-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2023 12 n/a-n/a |
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Nevena Zivanovic @@aut@@ Deniz Öner @@aut@@ Yann Abraham @@aut@@ Joseph McGinley @@aut@@ Simon B. Drysdale @@aut@@ Joanne G. Wildenbeest @@aut@@ Marjolein Crabbe @@aut@@ Greet Vanhoof @@aut@@ Kim Thys @@aut@@ Ryan S. Thwaites @@aut@@ Hannah Robinson @@aut@@ Louis Bont @@aut@@ Peter J. M. Openshaw @@aut@@ Federico Martinón‐Torres @@aut@@ RESCEU Investigators @@aut@@ Andrew J. Pollard @@aut@@ Jeroen Aerssens @@aut@@ |
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R5-920 Single‐cell immune profiling reveals markers of emergency myelopoiesis that distinguish severe from mild respiratory syncytial virus disease in infants |
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single‐cell immune profiling reveals markers of emergency myelopoiesis that distinguish severe from mild respiratory syncytial virus disease in infants |
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Single‐cell immune profiling reveals markers of emergency myelopoiesis that distinguish severe from mild respiratory syncytial virus disease in infants |
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Abstract Whereas most infants infected with respiratory syncytial virus (RSV) show no or only mild symptoms, an estimated 3 million children under five are hospitalized annually due to RSV disease. This study aimed to investigate biological mechanisms and associated biomarkers underlying RSV disease heterogeneity in young infants, enabling the potential to objectively categorize RSV‐infected infants according to their medical needs. Immunophenotypic and functional profiling demonstrated the emergence of immature and progenitor‐like neutrophils, proliferative monocytes (HLA‐DRLow, Ki67+), impaired antigen‐presenting function, downregulation of T cell response and low abundance of HLA‐DRLow B cells in severe RSV disease. HLA‐DRLow monocytes were found as a hallmark of RSV‐infected infants requiring hospitalization. Complementary transcriptomics identified genes associated with disease severity and pointed to the emergency myelopoiesis response. These results shed new light on mechanisms underlying the pathogenesis and development of severe RSV disease and identified potential new candidate biomarkers for patient stratification. |
abstractGer |
Abstract Whereas most infants infected with respiratory syncytial virus (RSV) show no or only mild symptoms, an estimated 3 million children under five are hospitalized annually due to RSV disease. This study aimed to investigate biological mechanisms and associated biomarkers underlying RSV disease heterogeneity in young infants, enabling the potential to objectively categorize RSV‐infected infants according to their medical needs. Immunophenotypic and functional profiling demonstrated the emergence of immature and progenitor‐like neutrophils, proliferative monocytes (HLA‐DRLow, Ki67+), impaired antigen‐presenting function, downregulation of T cell response and low abundance of HLA‐DRLow B cells in severe RSV disease. HLA‐DRLow monocytes were found as a hallmark of RSV‐infected infants requiring hospitalization. Complementary transcriptomics identified genes associated with disease severity and pointed to the emergency myelopoiesis response. These results shed new light on mechanisms underlying the pathogenesis and development of severe RSV disease and identified potential new candidate biomarkers for patient stratification. |
abstract_unstemmed |
Abstract Whereas most infants infected with respiratory syncytial virus (RSV) show no or only mild symptoms, an estimated 3 million children under five are hospitalized annually due to RSV disease. This study aimed to investigate biological mechanisms and associated biomarkers underlying RSV disease heterogeneity in young infants, enabling the potential to objectively categorize RSV‐infected infants according to their medical needs. Immunophenotypic and functional profiling demonstrated the emergence of immature and progenitor‐like neutrophils, proliferative monocytes (HLA‐DRLow, Ki67+), impaired antigen‐presenting function, downregulation of T cell response and low abundance of HLA‐DRLow B cells in severe RSV disease. HLA‐DRLow monocytes were found as a hallmark of RSV‐infected infants requiring hospitalization. Complementary transcriptomics identified genes associated with disease severity and pointed to the emergency myelopoiesis response. These results shed new light on mechanisms underlying the pathogenesis and development of severe RSV disease and identified potential new candidate biomarkers for patient stratification. |
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Single‐cell immune profiling reveals markers of emergency myelopoiesis that distinguish severe from mild respiratory syncytial virus disease in infants |
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