Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors

Autores
Nahmod, Karen Amelia; Gentilini, Ciara; Vermeulen, Elba Monica; Uharek, Lutz; Wang, Yong; Zhang, Jialin; Schultheiss, Heinz-Peter; Geffner, Jorge Raúl; Walther, Thomas
Año de publicación
2010
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Dendritic cells (DC) are highly specialized antigen-presenting cells with a unique ability to activate resting T lymphocytes and initiate primary immune responses. Angiotensin II (AII) is involved in key events of the inflammatory response. Because our previous work implicated an effect of AII on differentiation and function of murine and human DC, we investigated the impact of AII type 1 receptor (AT1) deficiency on the phenotypical and functional properties of mouse DC in vitro and in vivo. Bone marrow (BM) cells isolated from mice lacking AII subtype 1a receptor (AT1a), AII subtype 1b receptor (AT1b), or both receptor isoforms and control littermates [wild type (WT)] were cultured for 7 days in the presence of recombinant mouse granulocyte/macrophage colony-stimulating factor to generate myeloid DC in vitro. Generation of CD11c+ cells was less efficient in both AT1a- and AT1b-deficient BM cells than in WT BM cell cultures. Moreover, DC generated from AT1-deficient progenitors showed lower levels of expression of major histocompatibility complex II (MHC-II) and CD11c (p < 0.01) and a marked reduction in their allostimulatory activity (p < 0.01 or 0.001). Although AT1-deficient DC released comparable levels of interleukin (IL)-10 and IL-12p70 to WT DC, they produced significantly lower levels of tumor necrosis factor α (TNF-α) (p < 0.05). Remarkably, CD11c+ cells isolated from the spleen of AT1 knockout mice challenged with lipopolysaccharide in vivo up-regulated MHC-II, CD40, and CD80 as did WT, but released significantly lower levels of TNF-α (p < 0.01). These data provide clear evidence that AT1 controls differentiation and functionality of DC and thus may have a crucial impact on inflammatory processes where local angiotensinergic systems are known to be activated.
Fil: Nahmod, Karen Amelia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Gentilini, Ciara. Universität zu Berlin; Alemania
Fil: Vermeulen, Elba Monica. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Fil: Uharek, Lutz. Universität zu Berlin; Alemania
Fil: Wang, Yong. University of Hull; Reino Unido. Justus Liebig University Giessen; Alemania
Fil: Zhang, Jialin. Justus Liebig University Giessen; Alemania
Fil: Schultheiss, Heinz-Peter. Universität zu Berlin; Alemania
Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Fil: Walther, Thomas. University of Hull; Reino Unido. Justus Liebig University Giessen; Alemania
Materia
DENDRITIC CELLS
ANGIOTENSIN II
RECEPTOR ANGIOTENSIN TYPE 1
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:11336/96032
Acceder
id CONICETDig_6e51f94eb89ec2131c8d05d24b336e93
oai_identifier_str oai:ri.conicet.gov.ar:11336/96032
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 ReceptorsNahmod, Karen AmeliaGentilini, CiaraVermeulen, Elba MonicaUharek, LutzWang, YongZhang, JialinSchultheiss, Heinz-PeterGeffner, Jorge RaúlWalther, ThomasDENDRITIC CELLSANGIOTENSIN IIRECEPTOR ANGIOTENSIN TYPE 1https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Dendritic cells (DC) are highly specialized antigen-presenting cells with a unique ability to activate resting T lymphocytes and initiate primary immune responses. Angiotensin II (AII) is involved in key events of the inflammatory response. Because our previous work implicated an effect of AII on differentiation and function of murine and human DC, we investigated the impact of AII type 1 receptor (AT1) deficiency on the phenotypical and functional properties of mouse DC in vitro and in vivo. Bone marrow (BM) cells isolated from mice lacking AII subtype 1a receptor (AT1a), AII subtype 1b receptor (AT1b), or both receptor isoforms and control littermates [wild type (WT)] were cultured for 7 days in the presence of recombinant mouse granulocyte/macrophage colony-stimulating factor to generate myeloid DC in vitro. Generation of CD11c+ cells was less efficient in both AT1a- and AT1b-deficient BM cells than in WT BM cell cultures. Moreover, DC generated from AT1-deficient progenitors showed lower levels of expression of major histocompatibility complex II (MHC-II) and CD11c (p < 0.01) and a marked reduction in their allostimulatory activity (p < 0.01 or 0.001). Although AT1-deficient DC released comparable levels of interleukin (IL)-10 and IL-12p70 to WT DC, they produced significantly lower levels of tumor necrosis factor α (TNF-α) (p < 0.05). Remarkably, CD11c+ cells isolated from the spleen of AT1 knockout mice challenged with lipopolysaccharide in vivo up-regulated MHC-II, CD40, and CD80 as did WT, but released significantly lower levels of TNF-α (p < 0.01). These data provide clear evidence that AT1 controls differentiation and functionality of DC and thus may have a crucial impact on inflammatory processes where local angiotensinergic systems are known to be activated.Fil: Nahmod, Karen Amelia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Gentilini, Ciara. Universität zu Berlin; AlemaniaFil: Vermeulen, Elba Monica. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; ArgentinaFil: Uharek, Lutz. Universität zu Berlin; AlemaniaFil: Wang, Yong. University of Hull; Reino Unido. Justus Liebig University Giessen; AlemaniaFil: Zhang, Jialin. Justus Liebig University Giessen; AlemaniaFil: Schultheiss, Heinz-Peter. Universität zu Berlin; AlemaniaFil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; ArgentinaFil: Walther, Thomas. University of Hull; Reino Unido. Justus Liebig University Giessen; AlemaniaAmerican Society for Pharmacology and Experimental Therapeutics2010-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/96032Nahmod, Karen Amelia; Gentilini, Ciara; Vermeulen, Elba Monica; Uharek, Lutz; Wang, Yong; et al.; Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors; American Society for Pharmacology and Experimental Therapeutics; Journal of Pharmacology and Experimental Therapeutics; 334; 3; 9-2010; 854-8620022-3565CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://jpet.aspetjournals.org/content/334/3/854info:eu-repo/semantics/altIdentifier/doi/10.1124/jpet.109.161760info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:04:28Zoai:ri.conicet.gov.ar:11336/96032instacron: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 10:04:29.082CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors
title Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors
spellingShingle Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors
Nahmod, Karen Amelia
DENDRITIC CELLS
ANGIOTENSIN II
RECEPTOR ANGIOTENSIN TYPE 1
title_short Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors
title_full Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors
title_fullStr Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors
title_full_unstemmed Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors
title_sort Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors
dc.creator.none.fl_str_mv Nahmod, Karen Amelia
Gentilini, Ciara
Vermeulen, Elba Monica
Uharek, Lutz
Wang, Yong
Zhang, Jialin
Schultheiss, Heinz-Peter
Geffner, Jorge Raúl
Walther, Thomas
author Nahmod, Karen Amelia
author_facet Nahmod, Karen Amelia
Gentilini, Ciara
Vermeulen, Elba Monica
Uharek, Lutz
Wang, Yong
Zhang, Jialin
Schultheiss, Heinz-Peter
Geffner, Jorge Raúl
Walther, Thomas
author_role author
author2 Gentilini, Ciara
Vermeulen, Elba Monica
Uharek, Lutz
Wang, Yong
Zhang, Jialin
Schultheiss, Heinz-Peter
Geffner, Jorge Raúl
Walther, Thomas
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv DENDRITIC CELLS
ANGIOTENSIN II
RECEPTOR ANGIOTENSIN TYPE 1
topic DENDRITIC CELLS
ANGIOTENSIN II
RECEPTOR ANGIOTENSIN TYPE 1
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Dendritic cells (DC) are highly specialized antigen-presenting cells with a unique ability to activate resting T lymphocytes and initiate primary immune responses. Angiotensin II (AII) is involved in key events of the inflammatory response. Because our previous work implicated an effect of AII on differentiation and function of murine and human DC, we investigated the impact of AII type 1 receptor (AT1) deficiency on the phenotypical and functional properties of mouse DC in vitro and in vivo. Bone marrow (BM) cells isolated from mice lacking AII subtype 1a receptor (AT1a), AII subtype 1b receptor (AT1b), or both receptor isoforms and control littermates [wild type (WT)] were cultured for 7 days in the presence of recombinant mouse granulocyte/macrophage colony-stimulating factor to generate myeloid DC in vitro. Generation of CD11c+ cells was less efficient in both AT1a- and AT1b-deficient BM cells than in WT BM cell cultures. Moreover, DC generated from AT1-deficient progenitors showed lower levels of expression of major histocompatibility complex II (MHC-II) and CD11c (p < 0.01) and a marked reduction in their allostimulatory activity (p < 0.01 or 0.001). Although AT1-deficient DC released comparable levels of interleukin (IL)-10 and IL-12p70 to WT DC, they produced significantly lower levels of tumor necrosis factor α (TNF-α) (p < 0.05). Remarkably, CD11c+ cells isolated from the spleen of AT1 knockout mice challenged with lipopolysaccharide in vivo up-regulated MHC-II, CD40, and CD80 as did WT, but released significantly lower levels of TNF-α (p < 0.01). These data provide clear evidence that AT1 controls differentiation and functionality of DC and thus may have a crucial impact on inflammatory processes where local angiotensinergic systems are known to be activated.
Fil: Nahmod, Karen Amelia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Gentilini, Ciara. Universität zu Berlin; Alemania
Fil: Vermeulen, Elba Monica. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Fil: Uharek, Lutz. Universität zu Berlin; Alemania
Fil: Wang, Yong. University of Hull; Reino Unido. Justus Liebig University Giessen; Alemania
Fil: Zhang, Jialin. Justus Liebig University Giessen; Alemania
Fil: Schultheiss, Heinz-Peter. Universität zu Berlin; Alemania
Fil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Academia Nacional de Medicina de Buenos Aires; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Fil: Walther, Thomas. University of Hull; Reino Unido. Justus Liebig University Giessen; Alemania
description Dendritic cells (DC) are highly specialized antigen-presenting cells with a unique ability to activate resting T lymphocytes and initiate primary immune responses. Angiotensin II (AII) is involved in key events of the inflammatory response. Because our previous work implicated an effect of AII on differentiation and function of murine and human DC, we investigated the impact of AII type 1 receptor (AT1) deficiency on the phenotypical and functional properties of mouse DC in vitro and in vivo. Bone marrow (BM) cells isolated from mice lacking AII subtype 1a receptor (AT1a), AII subtype 1b receptor (AT1b), or both receptor isoforms and control littermates [wild type (WT)] were cultured for 7 days in the presence of recombinant mouse granulocyte/macrophage colony-stimulating factor to generate myeloid DC in vitro. Generation of CD11c+ cells was less efficient in both AT1a- and AT1b-deficient BM cells than in WT BM cell cultures. Moreover, DC generated from AT1-deficient progenitors showed lower levels of expression of major histocompatibility complex II (MHC-II) and CD11c (p < 0.01) and a marked reduction in their allostimulatory activity (p < 0.01 or 0.001). Although AT1-deficient DC released comparable levels of interleukin (IL)-10 and IL-12p70 to WT DC, they produced significantly lower levels of tumor necrosis factor α (TNF-α) (p < 0.05). Remarkably, CD11c+ cells isolated from the spleen of AT1 knockout mice challenged with lipopolysaccharide in vivo up-regulated MHC-II, CD40, and CD80 as did WT, but released significantly lower levels of TNF-α (p < 0.01). These data provide clear evidence that AT1 controls differentiation and functionality of DC and thus may have a crucial impact on inflammatory processes where local angiotensinergic systems are known to be activated.
publishDate 2010
dc.date.none.fl_str_mv 2010-09
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/11336/96032
Nahmod, Karen Amelia; Gentilini, Ciara; Vermeulen, Elba Monica; Uharek, Lutz; Wang, Yong; et al.; Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors; American Society for Pharmacology and Experimental Therapeutics; Journal of Pharmacology and Experimental Therapeutics; 334; 3; 9-2010; 854-862
0022-3565
CONICET Digital
CONICET
url http://hdl.handle.net/11336/96032
identifier_str_mv Nahmod, Karen Amelia; Gentilini, Ciara; Vermeulen, Elba Monica; Uharek, Lutz; Wang, Yong; et al.; Impaired Function of Dendritic Cells Deficient in Angiotensin II Type 1 Receptors; American Society for Pharmacology and Experimental Therapeutics; Journal of Pharmacology and Experimental Therapeutics; 334; 3; 9-2010; 854-862
0022-3565
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://jpet.aspetjournals.org/content/334/3/854
info:eu-repo/semantics/altIdentifier/doi/10.1124/jpet.109.161760
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
dc.publisher.none.fl_str_mv American Society for Pharmacology and Experimental Therapeutics
publisher.none.fl_str_mv American Society for Pharmacology and Experimental Therapeutics
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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score 13.13397

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