Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children

Autores
Raiden, Silvina Claudia; Pandolfi, Julieta Belen; Payaslian, Florencia Pía; Anderson, Mariana; Rivarola Martinez, Norma Gisele; Ferrero, Fernando Claudio; Urtasun, Marcela; Fainboim, Leonardo; Geffner, Jorge Raúl; Arruvito, Maria Lourdes
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Respiratory syncytial virus (RSV) is the main cause of viral lower respiratory tract illness in infancy and early childhood. Each year, RSV is estimated to cause 34 million cases of lung infection, and the deaths of up to 199 000 children under 5 years of age worldwide. Children are usually infected by RSV during the first year of life, and virtually all by 3 years of age. Although in most cases the infection induces mild illness of the upper airways, 2 to 5% experience a severe bronchiolitis which require hospitalization and respiratory support in an intensive care unit. These patients show later a high susceptibility to develop recurrent wheeze and asthma (1, 2). Our current understanding of the host response to RSV in humans remains rudimentary because most observations have been performed in animal models which do not adequately reflect the course of human infection (3, 4). There is compelling evidence, however, that the host immune response has a prominent role in the pathogenesis of severe RSV infection (3, 4). FOXP3+CD4+ regulatory T cells (Tregs) have emerged as the most important cells able to prevent potentially harmful immune responses (5). Observations made in animal models clearly demonstrated that Tregs play a critical role in controlling lung inflammation in the course of RSV infection (6-8). The presence and function of Tregs during human RSV infection have not been yet analyzed. We here show that severe RSV infection of young children induces the selective depletion of peripheral blood Tregs.
Fil: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
Fil: Pandolfi, Julieta Belen. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Payaslian, Florencia Pía. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Anderson, Mariana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina
Fil: Rivarola Martinez, Norma Gisele. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina
Fil: Ferrero, Fernando Claudio. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina
Fil: Urtasun, Marcela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Arruvito, Maria Lourdes. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Materia
Foxp3
Syncytial Virus
Infants
Inflammation
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/37334
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/37334
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young childrenRaiden, Silvina ClaudiaPandolfi, Julieta BelenPayaslian, Florencia PíaAnderson, MarianaRivarola Martinez, Norma GiseleFerrero, Fernando ClaudioUrtasun, MarcelaFainboim, LeonardoGeffner, Jorge RaúlArruvito, Maria LourdesFoxp3Syncytial VirusInfantsInflammationhttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Respiratory syncytial virus (RSV) is the main cause of viral lower respiratory tract illness in infancy and early childhood. Each year, RSV is estimated to cause 34 million cases of lung infection, and the deaths of up to 199 000 children under 5 years of age worldwide. Children are usually infected by RSV during the first year of life, and virtually all by 3 years of age. Although in most cases the infection induces mild illness of the upper airways, 2 to 5% experience a severe bronchiolitis which require hospitalization and respiratory support in an intensive care unit. These patients show later a high susceptibility to develop recurrent wheeze and asthma (1, 2). Our current understanding of the host response to RSV in humans remains rudimentary because most observations have been performed in animal models which do not adequately reflect the course of human infection (3, 4). There is compelling evidence, however, that the host immune response has a prominent role in the pathogenesis of severe RSV infection (3, 4). FOXP3+CD4+ regulatory T cells (Tregs) have emerged as the most important cells able to prevent potentially harmful immune responses (5). Observations made in animal models clearly demonstrated that Tregs play a critical role in controlling lung inflammation in the course of RSV infection (6-8). The presence and function of Tregs during human RSV infection have not been yet analyzed. We here show that severe RSV infection of young children induces the selective depletion of peripheral blood Tregs.Fil: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; ArgentinaFil: Pandolfi, Julieta Belen. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Payaslian, Florencia Pía. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Anderson, Mariana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); ArgentinaFil: Rivarola Martinez, Norma Gisele. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); ArgentinaFil: Ferrero, Fernando Claudio. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); ArgentinaFil: Urtasun, Marcela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Arruvito, Maria Lourdes. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaAmerican Thoracic Society2014-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/37334Raiden, Silvina Claudia; Pandolfi, Julieta Belen; Payaslian, Florencia Pía; Anderson, Mariana; Rivarola Martinez, Norma Gisele; et al.; Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children; American Thoracic Society; American Journal of Respiratory and Critical Care Medicine; 189; 7; 4-2014; 865-8681073-449XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.atsjournals.org/doi/abs/10.1164/rccm.201311-1977LEinfo:eu-repo/semantics/altIdentifier/doi/10.1164/rccm.201311-1977LEinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:00:16Zoai:ri.conicet.gov.ar:11336/37334instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:00:16.569CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children
title Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children
spellingShingle Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children
Raiden, Silvina Claudia
Foxp3
Syncytial Virus
Infants
Inflammation
title_short Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children
title_full Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children
title_fullStr Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children
title_full_unstemmed Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children
title_sort Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children
dc.creator.none.fl_str_mv Raiden, Silvina Claudia
Pandolfi, Julieta Belen
Payaslian, Florencia Pía
Anderson, Mariana
Rivarola Martinez, Norma Gisele
Ferrero, Fernando Claudio
Urtasun, Marcela
Fainboim, Leonardo
Geffner, Jorge Raúl
Arruvito, Maria Lourdes
author Raiden, Silvina Claudia
author_facet Raiden, Silvina Claudia
Pandolfi, Julieta Belen
Payaslian, Florencia Pía
Anderson, Mariana
Rivarola Martinez, Norma Gisele
Ferrero, Fernando Claudio
Urtasun, Marcela
Fainboim, Leonardo
Geffner, Jorge Raúl
Arruvito, Maria Lourdes
author_role author
author2 Pandolfi, Julieta Belen
Payaslian, Florencia Pía
Anderson, Mariana
Rivarola Martinez, Norma Gisele
Ferrero, Fernando Claudio
Urtasun, Marcela
Fainboim, Leonardo
Geffner, Jorge Raúl
Arruvito, Maria Lourdes
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Foxp3
Syncytial Virus
Infants
Inflammation
topic Foxp3
Syncytial Virus
Infants
Inflammation
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Respiratory syncytial virus (RSV) is the main cause of viral lower respiratory tract illness in infancy and early childhood. Each year, RSV is estimated to cause 34 million cases of lung infection, and the deaths of up to 199 000 children under 5 years of age worldwide. Children are usually infected by RSV during the first year of life, and virtually all by 3 years of age. Although in most cases the infection induces mild illness of the upper airways, 2 to 5% experience a severe bronchiolitis which require hospitalization and respiratory support in an intensive care unit. These patients show later a high susceptibility to develop recurrent wheeze and asthma (1, 2). Our current understanding of the host response to RSV in humans remains rudimentary because most observations have been performed in animal models which do not adequately reflect the course of human infection (3, 4). There is compelling evidence, however, that the host immune response has a prominent role in the pathogenesis of severe RSV infection (3, 4). FOXP3+CD4+ regulatory T cells (Tregs) have emerged as the most important cells able to prevent potentially harmful immune responses (5). Observations made in animal models clearly demonstrated that Tregs play a critical role in controlling lung inflammation in the course of RSV infection (6-8). The presence and function of Tregs during human RSV infection have not been yet analyzed. We here show that severe RSV infection of young children induces the selective depletion of peripheral blood Tregs.
Fil: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina
Fil: Pandolfi, Julieta Belen. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Payaslian, Florencia Pía. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Anderson, Mariana. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina
Fil: Rivarola Martinez, Norma Gisele. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina
Fil: Ferrero, Fernando Claudio. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina
Fil: Urtasun, Marcela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Fainboim, Leonardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Arruvito, Maria Lourdes. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
description Respiratory syncytial virus (RSV) is the main cause of viral lower respiratory tract illness in infancy and early childhood. Each year, RSV is estimated to cause 34 million cases of lung infection, and the deaths of up to 199 000 children under 5 years of age worldwide. Children are usually infected by RSV during the first year of life, and virtually all by 3 years of age. Although in most cases the infection induces mild illness of the upper airways, 2 to 5% experience a severe bronchiolitis which require hospitalization and respiratory support in an intensive care unit. These patients show later a high susceptibility to develop recurrent wheeze and asthma (1, 2). Our current understanding of the host response to RSV in humans remains rudimentary because most observations have been performed in animal models which do not adequately reflect the course of human infection (3, 4). There is compelling evidence, however, that the host immune response has a prominent role in the pathogenesis of severe RSV infection (3, 4). FOXP3+CD4+ regulatory T cells (Tregs) have emerged as the most important cells able to prevent potentially harmful immune responses (5). Observations made in animal models clearly demonstrated that Tregs play a critical role in controlling lung inflammation in the course of RSV infection (6-8). The presence and function of Tregs during human RSV infection have not been yet analyzed. We here show that severe RSV infection of young children induces the selective depletion of peripheral blood Tregs.
publishDate 2014
dc.date.none.fl_str_mv 2014-04
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/37334
Raiden, Silvina Claudia; Pandolfi, Julieta Belen; Payaslian, Florencia Pía; Anderson, Mariana; Rivarola Martinez, Norma Gisele; et al.; Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children; American Thoracic Society; American Journal of Respiratory and Critical Care Medicine; 189; 7; 4-2014; 865-868
1073-449X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/37334
identifier_str_mv Raiden, Silvina Claudia; Pandolfi, Julieta Belen; Payaslian, Florencia Pía; Anderson, Mariana; Rivarola Martinez, Norma Gisele; et al.; Depletion of circulating regulatory T cells during severe respiratory syncytial virus infection in young children; American Thoracic Society; American Journal of Respiratory and Critical Care Medicine; 189; 7; 4-2014; 865-868
1073-449X
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.atsjournals.org/doi/abs/10.1164/rccm.201311-1977LE
info:eu-repo/semantics/altIdentifier/doi/10.1164/rccm.201311-1977LE
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv American Thoracic Society
publisher.none.fl_str_mv American Thoracic Society
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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