Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease

Autores
Sananez, Inés; Raiden, Silvina Claudia; Erra Diaz, Fernando Alberto; De Lillo, Leonardo; Holgado, María Pía; Geffner, Jorge Raúl; Arruvito, Maria Lourdes
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background FOXP3 + regulatory T cells (Tregs) restrain the destructive potential of the immune system. We have previously reported a pronounced reduction in circulating Tregs in infants with severe respiratory syncytial virus (RSV) disease. Because interleukin-2 (IL-2) is critical for Treg growth, survival, and activity, we here analyzed IL-2 production and function in RSV-infected infants. Methods Phenotype, proliferation, IL-2 production, and IL-2 signaling in CD4 + T cells were analyzed by flow cytometry. Serum soluble CD25 levels were quantified by ELISA. Results CD4 + T cells from RSV-infected infants produced lower amounts of IL-2 and showed a reduced proliferative response compared with healthy infants. IL-2 increased CD4 + T-cell proliferation and FOXP3 expression in both healthy and RSV-infected infants. However, although IL-2 induced a similar pattern of STAT5 phosphorylation, the proliferative response of CD4 + T cells and the expression of FOXP3 + remained significantly lower in RSV-infected infants. Interestingly, we found a negative correlation between disease severity and both the production of IL-2 by CD4 + T cells and the ability of exogenous IL-2 to restore the pool of FOXP3 + CD4 + T cells. Conclusions A reduced ability to produce IL-2 and a limited response to this cytokine may affect the function of CD4 + T cells in RSV-infected infants.
Fil: Sananez, Inés. 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: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina
Fil: Erra Diaz, Fernando Alberto. 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: De Lillo, Leonardo. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina
Fil: Holgado, María Pía. 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: 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. 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
Materia
CD25
CD4 + T CELLS
FOXP3
IL-2
INFANTS
RESPIRATORY SYNCYTIAL VIRUS
SEVERE BRONCHIOLITIS
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:11336/87618
Acceder
id CONICETDig_5a3ab358de6eb36be6ff6a13317e5990
oai_identifier_str oai:ri.conicet.gov.ar:11336/87618
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus DiseaseSananez, InésRaiden, Silvina ClaudiaErra Diaz, Fernando AlbertoDe Lillo, LeonardoHolgado, María PíaGeffner, Jorge RaúlArruvito, Maria LourdesCD25CD4 + T CELLSFOXP3IL-2INFANTSRESPIRATORY SYNCYTIAL VIRUSSEVERE BRONCHIOLITIShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Background FOXP3 + regulatory T cells (Tregs) restrain the destructive potential of the immune system. We have previously reported a pronounced reduction in circulating Tregs in infants with severe respiratory syncytial virus (RSV) disease. Because interleukin-2 (IL-2) is critical for Treg growth, survival, and activity, we here analyzed IL-2 production and function in RSV-infected infants. Methods Phenotype, proliferation, IL-2 production, and IL-2 signaling in CD4 + T cells were analyzed by flow cytometry. Serum soluble CD25 levels were quantified by ELISA. Results CD4 + T cells from RSV-infected infants produced lower amounts of IL-2 and showed a reduced proliferative response compared with healthy infants. IL-2 increased CD4 + T-cell proliferation and FOXP3 expression in both healthy and RSV-infected infants. However, although IL-2 induced a similar pattern of STAT5 phosphorylation, the proliferative response of CD4 + T cells and the expression of FOXP3 + remained significantly lower in RSV-infected infants. Interestingly, we found a negative correlation between disease severity and both the production of IL-2 by CD4 + T cells and the ability of exogenous IL-2 to restore the pool of FOXP3 + CD4 + T cells. Conclusions A reduced ability to produce IL-2 and a limited response to this cytokine may affect the function of CD4 + T cells in RSV-infected infants.Fil: Sananez, Inés. 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: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); ArgentinaFil: Erra Diaz, Fernando Alberto. 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: De Lillo, Leonardo. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); ArgentinaFil: Holgado, María Pía. 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: 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. 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; ArgentinaUniversity of Chicago Press2018-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/87618Sananez, Inés; Raiden, Silvina Claudia; Erra Diaz, Fernando Alberto; De Lillo, Leonardo; Holgado, María Pía; et al.; Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease; University of Chicago Press; Journal Of Infectious Diseases; 218; 1; 6-2018; 75-830022-1899CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/jid/advance-article/doi/10.1093/infdis/jiy180/4955865info:eu-repo/semantics/altIdentifier/doi/10.1093/infdis/jiy180info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:45:20Zoai:ri.conicet.gov.ar:11336/87618instacron: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 09:45:20.518CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease
title Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease
spellingShingle Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease
Sananez, Inés
CD25
CD4 + T CELLS
FOXP3
IL-2
INFANTS
RESPIRATORY SYNCYTIAL VIRUS
SEVERE BRONCHIOLITIS
title_short Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease
title_full Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease
title_fullStr Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease
title_full_unstemmed Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease
title_sort Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease
dc.creator.none.fl_str_mv Sananez, Inés
Raiden, Silvina Claudia
Erra Diaz, Fernando Alberto
De Lillo, Leonardo
Holgado, María Pía
Geffner, Jorge Raúl
Arruvito, Maria Lourdes
author Sananez, Inés
author_facet Sananez, Inés
Raiden, Silvina Claudia
Erra Diaz, Fernando Alberto
De Lillo, Leonardo
Holgado, María Pía
Geffner, Jorge Raúl
Arruvito, Maria Lourdes
author_role author
author2 Raiden, Silvina Claudia
Erra Diaz, Fernando Alberto
De Lillo, Leonardo
Holgado, María Pía
Geffner, Jorge Raúl
Arruvito, Maria Lourdes
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv CD25
CD4 + T CELLS
FOXP3
IL-2
INFANTS
RESPIRATORY SYNCYTIAL VIRUS
SEVERE BRONCHIOLITIS
topic CD25
CD4 + T CELLS
FOXP3
IL-2
INFANTS
RESPIRATORY SYNCYTIAL VIRUS
SEVERE BRONCHIOLITIS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Background FOXP3 + regulatory T cells (Tregs) restrain the destructive potential of the immune system. We have previously reported a pronounced reduction in circulating Tregs in infants with severe respiratory syncytial virus (RSV) disease. Because interleukin-2 (IL-2) is critical for Treg growth, survival, and activity, we here analyzed IL-2 production and function in RSV-infected infants. Methods Phenotype, proliferation, IL-2 production, and IL-2 signaling in CD4 + T cells were analyzed by flow cytometry. Serum soluble CD25 levels were quantified by ELISA. Results CD4 + T cells from RSV-infected infants produced lower amounts of IL-2 and showed a reduced proliferative response compared with healthy infants. IL-2 increased CD4 + T-cell proliferation and FOXP3 expression in both healthy and RSV-infected infants. However, although IL-2 induced a similar pattern of STAT5 phosphorylation, the proliferative response of CD4 + T cells and the expression of FOXP3 + remained significantly lower in RSV-infected infants. Interestingly, we found a negative correlation between disease severity and both the production of IL-2 by CD4 + T cells and the ability of exogenous IL-2 to restore the pool of FOXP3 + CD4 + T cells. Conclusions A reduced ability to produce IL-2 and a limited response to this cytokine may affect the function of CD4 + T cells in RSV-infected infants.
Fil: Sananez, Inés. 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: Raiden, Silvina Claudia. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina
Fil: Erra Diaz, Fernando Alberto. 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: De Lillo, Leonardo. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); Argentina
Fil: Holgado, María Pía. 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: 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. 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
description Background FOXP3 + regulatory T cells (Tregs) restrain the destructive potential of the immune system. We have previously reported a pronounced reduction in circulating Tregs in infants with severe respiratory syncytial virus (RSV) disease. Because interleukin-2 (IL-2) is critical for Treg growth, survival, and activity, we here analyzed IL-2 production and function in RSV-infected infants. Methods Phenotype, proliferation, IL-2 production, and IL-2 signaling in CD4 + T cells were analyzed by flow cytometry. Serum soluble CD25 levels were quantified by ELISA. Results CD4 + T cells from RSV-infected infants produced lower amounts of IL-2 and showed a reduced proliferative response compared with healthy infants. IL-2 increased CD4 + T-cell proliferation and FOXP3 expression in both healthy and RSV-infected infants. However, although IL-2 induced a similar pattern of STAT5 phosphorylation, the proliferative response of CD4 + T cells and the expression of FOXP3 + remained significantly lower in RSV-infected infants. Interestingly, we found a negative correlation between disease severity and both the production of IL-2 by CD4 + T cells and the ability of exogenous IL-2 to restore the pool of FOXP3 + CD4 + T cells. Conclusions A reduced ability to produce IL-2 and a limited response to this cytokine may affect the function of CD4 + T cells in RSV-infected infants.
publishDate 2018
dc.date.none.fl_str_mv 2018-06
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/11336/87618
Sananez, Inés; Raiden, Silvina Claudia; Erra Diaz, Fernando Alberto; De Lillo, Leonardo; Holgado, María Pía; et al.; Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease; University of Chicago Press; Journal Of Infectious Diseases; 218; 1; 6-2018; 75-83
0022-1899
CONICET Digital
CONICET
url http://hdl.handle.net/11336/87618
identifier_str_mv Sananez, Inés; Raiden, Silvina Claudia; Erra Diaz, Fernando Alberto; De Lillo, Leonardo; Holgado, María Pía; et al.; Dampening of IL-2 Function in Infants with Severe Respiratory Syncytial Virus Disease; University of Chicago Press; Journal Of Infectious Diseases; 218; 1; 6-2018; 75-83
0022-1899
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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info:eu-repo/semantics/altIdentifier/doi/10.1093/infdis/jiy180
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
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dc.publisher.none.fl_str_mv University of Chicago Press
publisher.none.fl_str_mv University of Chicago Press
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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