ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis
- Autores
- Marchini, Timoteo Oscar; Hansen, Sophie; Wolf, Dennis
- Año de publicación
- 2021
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Atherosclerosis is a chronic inflammatory condition of the arterial wall that leads to the formation of vessel‐occluding plaques within the subintimal space of middle‐sized and larger arter-ies. While traditionally understood as a myeloid‐driven lipid‐storage disease, growing evidence suggests that the accumulation of low‐density lipoprotein cholesterol (LDL‐C) ignites an autoimmune response with CD4+ T‐helper (TH) cells that recognize self‐peptides from Apolipoprotein B (ApoB), the core protein of LDL‐C. These autoreactive CD4+ T cells home to the atherosclerotic plaque, clonally expand, instruct other cells in the plaque, and induce clinical plaque instability. Recent developments in detecting antigen‐specific cells at the single cell level have demonstrated that ApoB‐reactive CD4+ T cells exist in humans and mice. Their phenotypes and functions deviate from classical immunological concepts of distinct and terminally differentiated TH immunity. In-stead, ApoB‐specific CD4+ T cells have a highly plastic phenotype, can acquire several, partially opposing and mixed transcriptional programs simultaneously, and transit from one TH subset into another over time. In this review, we highlight adaptive immune mechanisms in atherosclerosis with a focus on CD4+ T cells, introduce novel technologies to detect ApoB‐specific CD4+ T cells at the single cell level, and discuss the potential impact of ApoB‐driven autoimmunity in atheroscle-rosis.
Fil: Marchini, Timoteo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Albert Ludwigs University of Freiburg; Alemania
Fil: Hansen, Sophie. Albert Ludwigs University of Freiburg; Alemania
Fil: Wolf, Dennis. Albert Ludwigs University of Freiburg; Alemania - Materia
-
APOLIPOPROTEIN B
ATHEROSCLEROSIS
AUTOIMMUNITY
IMMUNITY
LDL
T CELLS - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/179207
Ver los metadatos del registro completo
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ApoB-Specific CD4+ T Cells in Mouse and Human AtherosclerosisMarchini, Timoteo OscarHansen, SophieWolf, DennisAPOLIPOPROTEIN BATHEROSCLEROSISAUTOIMMUNITYIMMUNITYLDLT CELLShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Atherosclerosis is a chronic inflammatory condition of the arterial wall that leads to the formation of vessel‐occluding plaques within the subintimal space of middle‐sized and larger arter-ies. While traditionally understood as a myeloid‐driven lipid‐storage disease, growing evidence suggests that the accumulation of low‐density lipoprotein cholesterol (LDL‐C) ignites an autoimmune response with CD4+ T‐helper (TH) cells that recognize self‐peptides from Apolipoprotein B (ApoB), the core protein of LDL‐C. These autoreactive CD4+ T cells home to the atherosclerotic plaque, clonally expand, instruct other cells in the plaque, and induce clinical plaque instability. Recent developments in detecting antigen‐specific cells at the single cell level have demonstrated that ApoB‐reactive CD4+ T cells exist in humans and mice. Their phenotypes and functions deviate from classical immunological concepts of distinct and terminally differentiated TH immunity. In-stead, ApoB‐specific CD4+ T cells have a highly plastic phenotype, can acquire several, partially opposing and mixed transcriptional programs simultaneously, and transit from one TH subset into another over time. In this review, we highlight adaptive immune mechanisms in atherosclerosis with a focus on CD4+ T cells, introduce novel technologies to detect ApoB‐specific CD4+ T cells at the single cell level, and discuss the potential impact of ApoB‐driven autoimmunity in atheroscle-rosis.Fil: Marchini, Timoteo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Albert Ludwigs University of Freiburg; AlemaniaFil: Hansen, Sophie. Albert Ludwigs University of Freiburg; AlemaniaFil: Wolf, Dennis. Albert Ludwigs University of Freiburg; AlemaniaMDPI2021-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/179207Marchini, Timoteo Oscar; Hansen, Sophie; Wolf, Dennis; ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis; MDPI; Cells; 10; 2; 2-2021; 1-262073-4409CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/2073-4409/10/2/446info:eu-repo/semantics/altIdentifier/doi/10.3390/cells10020446info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:44:29Zoai:ri.conicet.gov.ar:11336/179207instacron: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 09:44:29.994CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis |
title |
ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis |
spellingShingle |
ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis Marchini, Timoteo Oscar APOLIPOPROTEIN B ATHEROSCLEROSIS AUTOIMMUNITY IMMUNITY LDL T CELLS |
title_short |
ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis |
title_full |
ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis |
title_fullStr |
ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis |
title_full_unstemmed |
ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis |
title_sort |
ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis |
dc.creator.none.fl_str_mv |
Marchini, Timoteo Oscar Hansen, Sophie Wolf, Dennis |
author |
Marchini, Timoteo Oscar |
author_facet |
Marchini, Timoteo Oscar Hansen, Sophie Wolf, Dennis |
author_role |
author |
author2 |
Hansen, Sophie Wolf, Dennis |
author2_role |
author author |
dc.subject.none.fl_str_mv |
APOLIPOPROTEIN B ATHEROSCLEROSIS AUTOIMMUNITY IMMUNITY LDL T CELLS |
topic |
APOLIPOPROTEIN B ATHEROSCLEROSIS AUTOIMMUNITY IMMUNITY LDL 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 |
Atherosclerosis is a chronic inflammatory condition of the arterial wall that leads to the formation of vessel‐occluding plaques within the subintimal space of middle‐sized and larger arter-ies. While traditionally understood as a myeloid‐driven lipid‐storage disease, growing evidence suggests that the accumulation of low‐density lipoprotein cholesterol (LDL‐C) ignites an autoimmune response with CD4+ T‐helper (TH) cells that recognize self‐peptides from Apolipoprotein B (ApoB), the core protein of LDL‐C. These autoreactive CD4+ T cells home to the atherosclerotic plaque, clonally expand, instruct other cells in the plaque, and induce clinical plaque instability. Recent developments in detecting antigen‐specific cells at the single cell level have demonstrated that ApoB‐reactive CD4+ T cells exist in humans and mice. Their phenotypes and functions deviate from classical immunological concepts of distinct and terminally differentiated TH immunity. In-stead, ApoB‐specific CD4+ T cells have a highly plastic phenotype, can acquire several, partially opposing and mixed transcriptional programs simultaneously, and transit from one TH subset into another over time. In this review, we highlight adaptive immune mechanisms in atherosclerosis with a focus on CD4+ T cells, introduce novel technologies to detect ApoB‐specific CD4+ T cells at the single cell level, and discuss the potential impact of ApoB‐driven autoimmunity in atheroscle-rosis. Fil: Marchini, Timoteo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Albert Ludwigs University of Freiburg; Alemania Fil: Hansen, Sophie. Albert Ludwigs University of Freiburg; Alemania Fil: Wolf, Dennis. Albert Ludwigs University of Freiburg; Alemania |
description |
Atherosclerosis is a chronic inflammatory condition of the arterial wall that leads to the formation of vessel‐occluding plaques within the subintimal space of middle‐sized and larger arter-ies. While traditionally understood as a myeloid‐driven lipid‐storage disease, growing evidence suggests that the accumulation of low‐density lipoprotein cholesterol (LDL‐C) ignites an autoimmune response with CD4+ T‐helper (TH) cells that recognize self‐peptides from Apolipoprotein B (ApoB), the core protein of LDL‐C. These autoreactive CD4+ T cells home to the atherosclerotic plaque, clonally expand, instruct other cells in the plaque, and induce clinical plaque instability. Recent developments in detecting antigen‐specific cells at the single cell level have demonstrated that ApoB‐reactive CD4+ T cells exist in humans and mice. Their phenotypes and functions deviate from classical immunological concepts of distinct and terminally differentiated TH immunity. In-stead, ApoB‐specific CD4+ T cells have a highly plastic phenotype, can acquire several, partially opposing and mixed transcriptional programs simultaneously, and transit from one TH subset into another over time. In this review, we highlight adaptive immune mechanisms in atherosclerosis with a focus on CD4+ T cells, introduce novel technologies to detect ApoB‐specific CD4+ T cells at the single cell level, and discuss the potential impact of ApoB‐driven autoimmunity in atheroscle-rosis. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-02 |
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/11336/179207 Marchini, Timoteo Oscar; Hansen, Sophie; Wolf, Dennis; ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis; MDPI; Cells; 10; 2; 2-2021; 1-26 2073-4409 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/179207 |
identifier_str_mv |
Marchini, Timoteo Oscar; Hansen, Sophie; Wolf, Dennis; ApoB-Specific CD4+ T Cells in Mouse and Human Atherosclerosis; MDPI; Cells; 10; 2; 2-2021; 1-26 2073-4409 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.mdpi.com/2073-4409/10/2/446 info:eu-repo/semantics/altIdentifier/doi/10.3390/cells10020446 |
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 |
dc.publisher.none.fl_str_mv |
MDPI |
publisher.none.fl_str_mv |
MDPI |
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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13.13397 |