ILC2 transfers to apolipoprotein E deficient mice reduce the lipid content of atherosclerotic lesions.
Alternatively activated macrophages
Anti-PC IgM
Apolipoprotein E deficient mice
Atherosclerosis
B1 cells
Eosinophils
IL-25
ILC2s
Journal
BMC immunology
ISSN: 1471-2172
Titre abrégé: BMC Immunol
Pays: England
ID NLM: 100966980
Informations de publication
Date de publication:
10 12 2019
10 12 2019
Historique:
received:
10
05
2018
accepted:
02
12
2019
entrez:
12
12
2019
pubmed:
12
12
2019
medline:
8
5
2020
Statut:
epublish
Résumé
Expansion of type 2 innate lymphoid cells (ILC2s) in hypercholesterolaemic mice protects against atherosclerosis while different ILC2 subsets have been described (natural, inflammatory) based on their suppression of tumorigenicity 2 (ST2) and killer-cell lectin like receptor G1 (KLRG1) expression. The aim of the current study is to characterize the interleukin 25 (IL25)-induced splenic ILC2 population (Lin Immunomagnetically enriched, FACS-sorted ILC2s from the spleens of IL-25 treated apoE With the current data we designate the IL25-induced ILC2 population to decrease the lipid content of atherosclerotic lesions in apoE
Sections du résumé
BACKGROUND
Expansion of type 2 innate lymphoid cells (ILC2s) in hypercholesterolaemic mice protects against atherosclerosis while different ILC2 subsets have been described (natural, inflammatory) based on their suppression of tumorigenicity 2 (ST2) and killer-cell lectin like receptor G1 (KLRG1) expression. The aim of the current study is to characterize the interleukin 25 (IL25)-induced splenic ILC2 population (Lin
RESULTS
Immunomagnetically enriched, FACS-sorted ILC2s from the spleens of IL-25 treated apoE
CONCLUSIONS
With the current data we designate the IL25-induced ILC2 population to decrease the lipid content of atherosclerotic lesions in apoE
Identifiants
pubmed: 31823769
doi: 10.1186/s12865-019-0330-z
pii: 10.1186/s12865-019-0330-z
pmc: PMC6905041
doi:
Substances chimiques
Apolipoproteins E
0
Biomarkers
0
Cytokines
0
Lipids
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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