Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection

Autores
Aoki, Maria del Pilar; Carrera Silva, Eugenio Antonio; Cuervo, Henar; Fresno, Manuel; Girones, Nuria; Gea, Susana
Año de publicación
2012
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Chagas myocarditis, which is caused by infection with the intracellular parasite Trypanosoma cruzi, remains the major infectious heart disease worldwide. Innate recognition through toll-like receptors (TLRs) on immune cells has not only been revealed to be critical for defense against T. cruzi but has also been involved in triggering the pathology. Subsequent studies revealed that this parasite activates nucleotide-binding oligomerization domain- (NOD-)like receptors and several particular transcription factors in TLR-independent manner. In addition to professional immune cells, T. cruzi infects and resides in different parenchyma cells. The innate receptors in nonimmune target tissues could also have an impact on host response. Thus, the outcome of the myocarditis or the inflamed liver relies on an intricate network of inflammatory mediators and signals given by immune and nonimmune cells. In this paper, we discuss the evidence of innate immunity to the parasite developed by the host, with emphasis on the crosstalk between immune and nonimmune cell responses.
Fil: Aoki, Maria del Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Carrera Silva, Eugenio Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Cuervo, Henar. Universidad Autónoma de Madrid; España
Fil: Fresno, Manuel. Universidad Autónoma de Madrid; España
Fil: Girones, Nuria. Universidad Autónoma de Madrid; España
Fil: Gea, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Materia
TRYPANOSOMA CRUZI INFECTION
INNATE IMMUNITY
CYTOKINES
NON IMMUNE CELLS
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:11336/54962

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spelling Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infectionAoki, Maria del PilarCarrera Silva, Eugenio AntonioCuervo, HenarFresno, ManuelGirones, NuriaGea, SusanaTRYPANOSOMA CRUZI INFECTIONINNATE IMMUNITYCYTOKINESNON IMMUNE CELLShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Chagas myocarditis, which is caused by infection with the intracellular parasite Trypanosoma cruzi, remains the major infectious heart disease worldwide. Innate recognition through toll-like receptors (TLRs) on immune cells has not only been revealed to be critical for defense against T. cruzi but has also been involved in triggering the pathology. Subsequent studies revealed that this parasite activates nucleotide-binding oligomerization domain- (NOD-)like receptors and several particular transcription factors in TLR-independent manner. In addition to professional immune cells, T. cruzi infects and resides in different parenchyma cells. The innate receptors in nonimmune target tissues could also have an impact on host response. Thus, the outcome of the myocarditis or the inflamed liver relies on an intricate network of inflammatory mediators and signals given by immune and nonimmune cells. In this paper, we discuss the evidence of innate immunity to the parasite developed by the host, with emphasis on the crosstalk between immune and nonimmune cell responses.Fil: Aoki, Maria del Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Carrera Silva, Eugenio Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Cuervo, Henar. Universidad Autónoma de Madrid; EspañaFil: Fresno, Manuel. Universidad Autónoma de Madrid; EspañaFil: Girones, Nuria. Universidad Autónoma de Madrid; EspañaFil: Gea, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaHindawi Publishing Corporation2012-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/54962Aoki, Maria del Pilar; Carrera Silva, Eugenio Antonio; Cuervo, Henar; Fresno, Manuel; Girones, Nuria; et al.; Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection; Hindawi Publishing Corporation; Journal of Parasitology Research; 2012; 8-2012; 1-132090-00312090-0031CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.hindawi.com/journals/jpr/2012/737324/info:eu-repo/semantics/altIdentifier/doi/10.1155/2012/737324info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:26:41Zoai:ri.conicet.gov.ar:11336/54962instacron: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:34982025-09-29 10:26:42.078CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection
title Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection
spellingShingle Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection
Aoki, Maria del Pilar
TRYPANOSOMA CRUZI INFECTION
INNATE IMMUNITY
CYTOKINES
NON IMMUNE CELLS
title_short Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection
title_full Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection
title_fullStr Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection
title_full_unstemmed Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection
title_sort Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection
dc.creator.none.fl_str_mv Aoki, Maria del Pilar
Carrera Silva, Eugenio Antonio
Cuervo, Henar
Fresno, Manuel
Girones, Nuria
Gea, Susana
author Aoki, Maria del Pilar
author_facet Aoki, Maria del Pilar
Carrera Silva, Eugenio Antonio
Cuervo, Henar
Fresno, Manuel
Girones, Nuria
Gea, Susana
author_role author
author2 Carrera Silva, Eugenio Antonio
Cuervo, Henar
Fresno, Manuel
Girones, Nuria
Gea, Susana
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv TRYPANOSOMA CRUZI INFECTION
INNATE IMMUNITY
CYTOKINES
NON IMMUNE CELLS
topic TRYPANOSOMA CRUZI INFECTION
INNATE IMMUNITY
CYTOKINES
NON IMMUNE CELLS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Chagas myocarditis, which is caused by infection with the intracellular parasite Trypanosoma cruzi, remains the major infectious heart disease worldwide. Innate recognition through toll-like receptors (TLRs) on immune cells has not only been revealed to be critical for defense against T. cruzi but has also been involved in triggering the pathology. Subsequent studies revealed that this parasite activates nucleotide-binding oligomerization domain- (NOD-)like receptors and several particular transcription factors in TLR-independent manner. In addition to professional immune cells, T. cruzi infects and resides in different parenchyma cells. The innate receptors in nonimmune target tissues could also have an impact on host response. Thus, the outcome of the myocarditis or the inflamed liver relies on an intricate network of inflammatory mediators and signals given by immune and nonimmune cells. In this paper, we discuss the evidence of innate immunity to the parasite developed by the host, with emphasis on the crosstalk between immune and nonimmune cell responses.
Fil: Aoki, Maria del Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Carrera Silva, Eugenio Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Cuervo, Henar. Universidad Autónoma de Madrid; España
Fil: Fresno, Manuel. Universidad Autónoma de Madrid; España
Fil: Girones, Nuria. Universidad Autónoma de Madrid; España
Fil: Gea, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
description Chagas myocarditis, which is caused by infection with the intracellular parasite Trypanosoma cruzi, remains the major infectious heart disease worldwide. Innate recognition through toll-like receptors (TLRs) on immune cells has not only been revealed to be critical for defense against T. cruzi but has also been involved in triggering the pathology. Subsequent studies revealed that this parasite activates nucleotide-binding oligomerization domain- (NOD-)like receptors and several particular transcription factors in TLR-independent manner. In addition to professional immune cells, T. cruzi infects and resides in different parenchyma cells. The innate receptors in nonimmune target tissues could also have an impact on host response. Thus, the outcome of the myocarditis or the inflamed liver relies on an intricate network of inflammatory mediators and signals given by immune and nonimmune cells. In this paper, we discuss the evidence of innate immunity to the parasite developed by the host, with emphasis on the crosstalk between immune and nonimmune cell responses.
publishDate 2012
dc.date.none.fl_str_mv 2012-08
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/11336/54962
Aoki, Maria del Pilar; Carrera Silva, Eugenio Antonio; Cuervo, Henar; Fresno, Manuel; Girones, Nuria; et al.; Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection; Hindawi Publishing Corporation; Journal of Parasitology Research; 2012; 8-2012; 1-13
2090-0031
2090-0031
CONICET Digital
CONICET
url http://hdl.handle.net/11336/54962
identifier_str_mv Aoki, Maria del Pilar; Carrera Silva, Eugenio Antonio; Cuervo, Henar; Fresno, Manuel; Girones, Nuria; et al.; Nonimmune cells contribute to crosstalk between immune cells and inflammatory mediators in the innate response to Trypanosoma cruzi infection; Hindawi Publishing Corporation; Journal of Parasitology Research; 2012; 8-2012; 1-13
2090-0031
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.hindawi.com/journals/jpr/2012/737324/
info:eu-repo/semantics/altIdentifier/doi/10.1155/2012/737324
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
dc.publisher.none.fl_str_mv Hindawi Publishing Corporation
publisher.none.fl_str_mv Hindawi Publishing Corporation
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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