The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses

Autores
Kiprina, Anastasiia; Teichmann, Tom; Martín Giménez, Virna Margarita; Xu, Wenqing; Sailer, Fiona; Windbergs, Maike; Manucha, Walter Ariel Fernando; Weigert, Andreas; Brandes, Ralf P.
Año de publicación
2024
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Anandamide (AEA) is an endocannabinoid that has recently been recognized as a regulator of various inflammatory diseases as well as cancer. While AEA was thought to predominantly engage cannabinoid (CB) receptors, recent findings suggest that, given its protective anti-inflammatory role in pathological conditions, anandamide may engage not only CB receptors. In this study, wesought to understand the role of exogenous AEA in a mouse model of acute inflammation. We found that AEA decreases the acute infiltration of myeloid cells including granulocytes and monocytes into the inflamed area, but unexpectedly increases the number of T cells at the site of inflammation. This was related to AEA signaling through nuclear receptor subfamily 4A (NR4A) transcription factors rather than CB receptors.Exploring regulatory mechanisms in the human system, we found that AEA broadly inhibits the migratory capacity of immune cells arguing for blocked emigration of T cells from the inflamed tissue. Taking a closer look at the impact of AEA on T cells revealed that AEA profoundly alters the activation and exhaustion status of CD4+ T and CD8+ T cells, thereby strongly inhibiting TH17 responses, while not altering TH1 differentiation. These data suggest that AEA has the potential to block chronic inflammation without influencing crucial anti-viral and anti-microbial immune defense mechanisms, and may therefore be an attractive molecule to interfere with the establishment of chronic inflammation.
Fil: Kiprina, Anastasiia. Goethe Universitat Frankfurt; Alemania
Fil: Teichmann, Tom. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research; Alemania
Fil: Martín Giménez, Virna Margarita. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Catolica de Cuyo - Sede San Juan. Facultad de Ciencias de la Alimentación, Bioquímicas y Farmacéuticas. Instituto de Investigación en Ciencias Químicas; Argentina
Fil: Xu, Wenqing. Goethe Universitat Frankfurt; Alemania
Fil: Sailer, Fiona. Goethe Universitat Frankfurt; Alemania
Fil: Windbergs, Maike. Goethe Universitat Frankfurt; Alemania
Fil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Departamento de Patología; Argentina
Fil: Weigert, Andreas. Goethe Universitat Frankfurt; Alemania
Fil: Brandes, Ralf P.. Goethe Universitat Frankfurt; Alemania
Materia
ANANDAMIDE
ENDOCANNABINOIDS
INFLAMMATION
T CELLS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/266560
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responsesKiprina, AnastasiiaTeichmann, TomMartín Giménez, Virna MargaritaXu, WenqingSailer, FionaWindbergs, MaikeManucha, Walter Ariel FernandoWeigert, AndreasBrandes, Ralf P.ANANDAMIDEENDOCANNABINOIDSINFLAMMATIONT CELLShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Anandamide (AEA) is an endocannabinoid that has recently been recognized as a regulator of various inflammatory diseases as well as cancer. While AEA was thought to predominantly engage cannabinoid (CB) receptors, recent findings suggest that, given its protective anti-inflammatory role in pathological conditions, anandamide may engage not only CB receptors. In this study, wesought to understand the role of exogenous AEA in a mouse model of acute inflammation. We found that AEA decreases the acute infiltration of myeloid cells including granulocytes and monocytes into the inflamed area, but unexpectedly increases the number of T cells at the site of inflammation. This was related to AEA signaling through nuclear receptor subfamily 4A (NR4A) transcription factors rather than CB receptors.Exploring regulatory mechanisms in the human system, we found that AEA broadly inhibits the migratory capacity of immune cells arguing for blocked emigration of T cells from the inflamed tissue. Taking a closer look at the impact of AEA on T cells revealed that AEA profoundly alters the activation and exhaustion status of CD4+ T and CD8+ T cells, thereby strongly inhibiting TH17 responses, while not altering TH1 differentiation. These data suggest that AEA has the potential to block chronic inflammation without influencing crucial anti-viral and anti-microbial immune defense mechanisms, and may therefore be an attractive molecule to interfere with the establishment of chronic inflammation.Fil: Kiprina, Anastasiia. Goethe Universitat Frankfurt; AlemaniaFil: Teichmann, Tom. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research; AlemaniaFil: Martín Giménez, Virna Margarita. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Catolica de Cuyo - Sede San Juan. Facultad de Ciencias de la Alimentación, Bioquímicas y Farmacéuticas. Instituto de Investigación en Ciencias Químicas; ArgentinaFil: Xu, Wenqing. Goethe Universitat Frankfurt; AlemaniaFil: Sailer, Fiona. Goethe Universitat Frankfurt; AlemaniaFil: Windbergs, Maike. Goethe Universitat Frankfurt; AlemaniaFil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Departamento de Patología; ArgentinaFil: Weigert, Andreas. Goethe Universitat Frankfurt; AlemaniaFil: Brandes, Ralf P.. Goethe Universitat Frankfurt; AlemaniaFrontiers Media2024-12info: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/11336/266560Kiprina, Anastasiia; Teichmann, Tom; Martín Giménez, Virna Margarita; Xu, Wenqing; Sailer, Fiona; et al.; The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses; Frontiers Media; Frontiers in Pharmacology; 15; 12-2024; 1-151663-9812CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2024.1528759/fullinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fphar.2024.1528759info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:10:25Zoai:ri.conicet.gov.ar:11336/266560instacron: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 10:10:25.571CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses
title The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses
spellingShingle The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses
Kiprina, Anastasiia
ANANDAMIDE
ENDOCANNABINOIDS
INFLAMMATION
T CELLS
title_short The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses
title_full The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses
title_fullStr The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses
title_full_unstemmed The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses
title_sort The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses
dc.creator.none.fl_str_mv Kiprina, Anastasiia
Teichmann, Tom
Martín Giménez, Virna Margarita
Xu, Wenqing
Sailer, Fiona
Windbergs, Maike
Manucha, Walter Ariel Fernando
Weigert, Andreas
Brandes, Ralf P.
author Kiprina, Anastasiia
author_facet Kiprina, Anastasiia
Teichmann, Tom
Martín Giménez, Virna Margarita
Xu, Wenqing
Sailer, Fiona
Windbergs, Maike
Manucha, Walter Ariel Fernando
Weigert, Andreas
Brandes, Ralf P.
author_role author
author2 Teichmann, Tom
Martín Giménez, Virna Margarita
Xu, Wenqing
Sailer, Fiona
Windbergs, Maike
Manucha, Walter Ariel Fernando
Weigert, Andreas
Brandes, Ralf P.
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv ANANDAMIDE
ENDOCANNABINOIDS
INFLAMMATION
T CELLS
topic ANANDAMIDE
ENDOCANNABINOIDS
INFLAMMATION
T 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 Anandamide (AEA) is an endocannabinoid that has recently been recognized as a regulator of various inflammatory diseases as well as cancer. While AEA was thought to predominantly engage cannabinoid (CB) receptors, recent findings suggest that, given its protective anti-inflammatory role in pathological conditions, anandamide may engage not only CB receptors. In this study, wesought to understand the role of exogenous AEA in a mouse model of acute inflammation. We found that AEA decreases the acute infiltration of myeloid cells including granulocytes and monocytes into the inflamed area, but unexpectedly increases the number of T cells at the site of inflammation. This was related to AEA signaling through nuclear receptor subfamily 4A (NR4A) transcription factors rather than CB receptors.Exploring regulatory mechanisms in the human system, we found that AEA broadly inhibits the migratory capacity of immune cells arguing for blocked emigration of T cells from the inflamed tissue. Taking a closer look at the impact of AEA on T cells revealed that AEA profoundly alters the activation and exhaustion status of CD4+ T and CD8+ T cells, thereby strongly inhibiting TH17 responses, while not altering TH1 differentiation. These data suggest that AEA has the potential to block chronic inflammation without influencing crucial anti-viral and anti-microbial immune defense mechanisms, and may therefore be an attractive molecule to interfere with the establishment of chronic inflammation.
Fil: Kiprina, Anastasiia. Goethe Universitat Frankfurt; Alemania
Fil: Teichmann, Tom. Goethe Universitat Frankfurt; Alemania. German Centre of Cardiovascular Research; Alemania
Fil: Martín Giménez, Virna Margarita. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Catolica de Cuyo - Sede San Juan. Facultad de Ciencias de la Alimentación, Bioquímicas y Farmacéuticas. Instituto de Investigación en Ciencias Químicas; Argentina
Fil: Xu, Wenqing. Goethe Universitat Frankfurt; Alemania
Fil: Sailer, Fiona. Goethe Universitat Frankfurt; Alemania
Fil: Windbergs, Maike. Goethe Universitat Frankfurt; Alemania
Fil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Departamento de Patología; Argentina
Fil: Weigert, Andreas. Goethe Universitat Frankfurt; Alemania
Fil: Brandes, Ralf P.. Goethe Universitat Frankfurt; Alemania
description Anandamide (AEA) is an endocannabinoid that has recently been recognized as a regulator of various inflammatory diseases as well as cancer. While AEA was thought to predominantly engage cannabinoid (CB) receptors, recent findings suggest that, given its protective anti-inflammatory role in pathological conditions, anandamide may engage not only CB receptors. In this study, wesought to understand the role of exogenous AEA in a mouse model of acute inflammation. We found that AEA decreases the acute infiltration of myeloid cells including granulocytes and monocytes into the inflamed area, but unexpectedly increases the number of T cells at the site of inflammation. This was related to AEA signaling through nuclear receptor subfamily 4A (NR4A) transcription factors rather than CB receptors.Exploring regulatory mechanisms in the human system, we found that AEA broadly inhibits the migratory capacity of immune cells arguing for blocked emigration of T cells from the inflamed tissue. Taking a closer look at the impact of AEA on T cells revealed that AEA profoundly alters the activation and exhaustion status of CD4+ T and CD8+ T cells, thereby strongly inhibiting TH17 responses, while not altering TH1 differentiation. These data suggest that AEA has the potential to block chronic inflammation without influencing crucial anti-viral and anti-microbial immune defense mechanisms, and may therefore be an attractive molecule to interfere with the establishment of chronic inflammation.
publishDate 2024
dc.date.none.fl_str_mv 2024-12
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/11336/266560
Kiprina, Anastasiia; Teichmann, Tom; Martín Giménez, Virna Margarita; Xu, Wenqing; Sailer, Fiona; et al.; The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses; Frontiers Media; Frontiers in Pharmacology; 15; 12-2024; 1-15
1663-9812
CONICET Digital
CONICET
url http://hdl.handle.net/11336/266560
identifier_str_mv Kiprina, Anastasiia; Teichmann, Tom; Martín Giménez, Virna Margarita; Xu, Wenqing; Sailer, Fiona; et al.; The endocannabinoid anandamide prevents TH17 programming of activated T lymphocytes while preserving TH1 responses; Frontiers Media; Frontiers in Pharmacology; 15; 12-2024; 1-15
1663-9812
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.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2024.1528759/full
info:eu-repo/semantics/altIdentifier/doi/10.3389/fphar.2024.1528759
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Frontiers Media
publisher.none.fl_str_mv Frontiers Media
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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