Immunity and Inflammation in Atherosclerosis.


Journal

Circulation research
ISSN: 1524-4571
Titre abrégé: Circ Res
Pays: United States
ID NLM: 0047103

Informations de publication

Date de publication:
18 01 2019
Historique:
entrez: 18 1 2019
pubmed: 18 1 2019
medline: 19 11 2019
Statut: ppublish

Résumé

There is now overwhelming experimental and clinical evidence that atherosclerosis is a chronic inflammatory disease. Lessons from genome-wide association studies, advanced in vivo imaging techniques, transgenic lineage tracing mice, and clinical interventional studies have shown that both innate and adaptive immune mechanisms can accelerate or curb atherosclerosis. Here, we summarize and discuss the pathogenesis of atherosclerosis with a focus on adaptive immunity. We discuss some limitations of animal models and the need for models that are tailored to better translate to human atherosclerosis and ultimately progress in prevention and treatment.

Identifiants

pubmed: 30653442
doi: 10.1161/CIRCRESAHA.118.313591
pmc: PMC6342482
mid: NIHMS1517398
doi:

Substances chimiques

Inflammation Mediators 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

315-327

Subventions

Organisme : NHLBI NIH HHS
ID : P01 HL088093
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL115232
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL121697
Pays : United States
Organisme : NHLBI NIH HHS
ID : R35 HL145241
Pays : United States

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Auteurs

Dennis Wolf (D)

From the Department of Cardiology and Angiology I, University Heart Center Freiburg, Germany (D.W.).
Faculty of Medicine, University of Freiburg, Germany (D.W.).

Klaus Ley (K)

Division of Inflammation Biology, La Jolla Institute for Immunology, CA (K.L.).
Department of Bioengineering, University of California San Diego, La Jolla (K.L.).

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Classifications MeSH