MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection

Autores
Berod, Luciana; Stüve, Philipp; Swallow, Maxine; Arnold Schrauf, Catharina; Kruse, Friederike; Gentilini, Maria Virginia; Freitag, Jenny; Holzmann, Bernhard; Sparwasser, Tim
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis that is responsible for almost 1.5 million deaths per year. Sensing of mycobacteria by the host's immune system relies on different families of receptors present on innate immune cells. Amongst them, several members of the TLR family are involved in the activation of immune cells by mycobacteria, yet the in vivo contribution of individual TLRs to the protective immune response remains controversial. On the contrary, MyD88, the adaptor molecule for most TLRs, plays a non-redundant role in the protection against tuberculosis and mice with a complete germline deletion of MyD88 succumb very early to infection. MyD88 is expressed in both immune and non-immune cells, but it is not clear whether control of mycobacteria requires ubiquitous or cell-type specific MyD88 expression. Therefore, using novel conditional switch-on mouse models, we aimed to investigate the importance of MyD88 signalling in DCs and macrophages for the induction of protective effector mechanisms against mycobacterial infection. We conclude that specific reactivation of MyD88 signalling in CD11c- or lysozyme M-expressing myeloid cells during Mycobacterium bovis Bacille Calmette-Guerin infection is sufficient to restore systemic and local inflammatory cytokine production and to control pathogen burden.
Fil: Berod, Luciana. Helmholtz Centre for Infection Research; Alemania. Medical School Hanover; Alemania
Fil: Stüve, Philipp. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Swallow, Maxine. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Arnold Schrauf, Catharina. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Kruse, Friederike. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Gentilini, Maria Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Helmholtz Centre for Infection Research; Alemania. Medical School Hanover; Alemania
Fil: Freitag, Jenny. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Holzmann, Bernhard. Universitat Technical Zu Munich; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Sparwasser, Tim. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Materia
Dendritic cells
Macrophages
Mycobacteria
MyD88
Conditional switch-on mice
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/18643
Acceder
id CONICETDig_45b305dfbd65a802d812936528daa5e5
oai_identifier_str oai:ri.conicet.gov.ar:11336/18643
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infectionBerod, LucianaStüve, PhilippSwallow, MaxineArnold Schrauf, CatharinaKruse, FriederikeGentilini, Maria VirginiaFreitag, JennyHolzmann, BernhardSparwasser, TimDendritic cellsMacrophagesMycobacteriaMyD88Conditional switch-on micehttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis that is responsible for almost 1.5 million deaths per year. Sensing of mycobacteria by the host's immune system relies on different families of receptors present on innate immune cells. Amongst them, several members of the TLR family are involved in the activation of immune cells by mycobacteria, yet the in vivo contribution of individual TLRs to the protective immune response remains controversial. On the contrary, MyD88, the adaptor molecule for most TLRs, plays a non-redundant role in the protection against tuberculosis and mice with a complete germline deletion of MyD88 succumb very early to infection. MyD88 is expressed in both immune and non-immune cells, but it is not clear whether control of mycobacteria requires ubiquitous or cell-type specific MyD88 expression. Therefore, using novel conditional switch-on mouse models, we aimed to investigate the importance of MyD88 signalling in DCs and macrophages for the induction of protective effector mechanisms against mycobacterial infection. We conclude that specific reactivation of MyD88 signalling in CD11c- or lysozyme M-expressing myeloid cells during Mycobacterium bovis Bacille Calmette-Guerin infection is sufficient to restore systemic and local inflammatory cytokine production and to control pathogen burden.Fil: Berod, Luciana. Helmholtz Centre for Infection Research; Alemania. Medical School Hanover; AlemaniaFil: Stüve, Philipp. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; AlemaniaFil: Swallow, Maxine. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; AlemaniaFil: Arnold Schrauf, Catharina. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; AlemaniaFil: Kruse, Friederike. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; AlemaniaFil: Gentilini, Maria Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Helmholtz Centre for Infection Research; Alemania. Medical School Hanover; AlemaniaFil: Freitag, Jenny. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; AlemaniaFil: Holzmann, Bernhard. Universitat Technical Zu Munich; Alemania. Helmholtz Centre for Infection Research; AlemaniaFil: Sparwasser, Tim. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; AlemaniaWiley VCH Verlag2014-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/18643Berod, Luciana; Stüve, Philipp; Swallow, Maxine; Arnold Schrauf, Catharina; Kruse, Friederike; et al.; MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection; Wiley VCH Verlag; European Journal of Immunology; 44; 5; 5-2014; 1399-14090014-29801521-4141CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1002/eji.201344039/abstractinfo:eu-repo/semantics/altIdentifier/doi/10.1002/eji.201344039info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:31:02Zoai:ri.conicet.gov.ar:11336/18643instacron: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 10:31:02.784CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection
title MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection
spellingShingle MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection
Berod, Luciana
Dendritic cells
Macrophages
Mycobacteria
MyD88
Conditional switch-on mice
title_short MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection
title_full MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection
title_fullStr MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection
title_full_unstemmed MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection
title_sort MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection
dc.creator.none.fl_str_mv Berod, Luciana
Stüve, Philipp
Swallow, Maxine
Arnold Schrauf, Catharina
Kruse, Friederike
Gentilini, Maria Virginia
Freitag, Jenny
Holzmann, Bernhard
Sparwasser, Tim
author Berod, Luciana
author_facet Berod, Luciana
Stüve, Philipp
Swallow, Maxine
Arnold Schrauf, Catharina
Kruse, Friederike
Gentilini, Maria Virginia
Freitag, Jenny
Holzmann, Bernhard
Sparwasser, Tim
author_role author
author2 Stüve, Philipp
Swallow, Maxine
Arnold Schrauf, Catharina
Kruse, Friederike
Gentilini, Maria Virginia
Freitag, Jenny
Holzmann, Bernhard
Sparwasser, Tim
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Dendritic cells
Macrophages
Mycobacteria
MyD88
Conditional switch-on mice
topic Dendritic cells
Macrophages
Mycobacteria
MyD88
Conditional switch-on mice
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis that is responsible for almost 1.5 million deaths per year. Sensing of mycobacteria by the host's immune system relies on different families of receptors present on innate immune cells. Amongst them, several members of the TLR family are involved in the activation of immune cells by mycobacteria, yet the in vivo contribution of individual TLRs to the protective immune response remains controversial. On the contrary, MyD88, the adaptor molecule for most TLRs, plays a non-redundant role in the protection against tuberculosis and mice with a complete germline deletion of MyD88 succumb very early to infection. MyD88 is expressed in both immune and non-immune cells, but it is not clear whether control of mycobacteria requires ubiquitous or cell-type specific MyD88 expression. Therefore, using novel conditional switch-on mouse models, we aimed to investigate the importance of MyD88 signalling in DCs and macrophages for the induction of protective effector mechanisms against mycobacterial infection. We conclude that specific reactivation of MyD88 signalling in CD11c- or lysozyme M-expressing myeloid cells during Mycobacterium bovis Bacille Calmette-Guerin infection is sufficient to restore systemic and local inflammatory cytokine production and to control pathogen burden.
Fil: Berod, Luciana. Helmholtz Centre for Infection Research; Alemania. Medical School Hanover; Alemania
Fil: Stüve, Philipp. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Swallow, Maxine. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Arnold Schrauf, Catharina. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Kruse, Friederike. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Gentilini, Maria Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Helmholtz Centre for Infection Research; Alemania. Medical School Hanover; Alemania
Fil: Freitag, Jenny. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Holzmann, Bernhard. Universitat Technical Zu Munich; Alemania. Helmholtz Centre for Infection Research; Alemania
Fil: Sparwasser, Tim. Medical School Hanover; Alemania. Helmholtz Centre for Infection Research; Alemania
description Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis that is responsible for almost 1.5 million deaths per year. Sensing of mycobacteria by the host's immune system relies on different families of receptors present on innate immune cells. Amongst them, several members of the TLR family are involved in the activation of immune cells by mycobacteria, yet the in vivo contribution of individual TLRs to the protective immune response remains controversial. On the contrary, MyD88, the adaptor molecule for most TLRs, plays a non-redundant role in the protection against tuberculosis and mice with a complete germline deletion of MyD88 succumb very early to infection. MyD88 is expressed in both immune and non-immune cells, but it is not clear whether control of mycobacteria requires ubiquitous or cell-type specific MyD88 expression. Therefore, using novel conditional switch-on mouse models, we aimed to investigate the importance of MyD88 signalling in DCs and macrophages for the induction of protective effector mechanisms against mycobacterial infection. We conclude that specific reactivation of MyD88 signalling in CD11c- or lysozyme M-expressing myeloid cells during Mycobacterium bovis Bacille Calmette-Guerin infection is sufficient to restore systemic and local inflammatory cytokine production and to control pathogen burden.
publishDate 2014
dc.date.none.fl_str_mv 2014-05
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/11336/18643
Berod, Luciana; Stüve, Philipp; Swallow, Maxine; Arnold Schrauf, Catharina; Kruse, Friederike; et al.; MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection; Wiley VCH Verlag; European Journal of Immunology; 44; 5; 5-2014; 1399-1409
0014-2980
1521-4141
CONICET Digital
CONICET
url http://hdl.handle.net/11336/18643
identifier_str_mv Berod, Luciana; Stüve, Philipp; Swallow, Maxine; Arnold Schrauf, Catharina; Kruse, Friederike; et al.; MyD88 signalling in myeloid cells is sufficient to prevent chronic mycobacterial infection; Wiley VCH Verlag; European Journal of Immunology; 44; 5; 5-2014; 1399-1409
0014-2980
1521-4141
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://onlinelibrary.wiley.com/doi/10.1002/eji.201344039/abstract
info:eu-repo/semantics/altIdentifier/doi/10.1002/eji.201344039
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley VCH Verlag
publisher.none.fl_str_mv Wiley VCH Verlag
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
_version_ 1844614319733473280
score 13.070432

Publicaciones similares