Follicular regulatory helper T cells control the response of regulatory B cells to a high-cholesterol diet.
Adoptive Transfer
Animals
Aorta
/ immunology
Aortic Diseases
/ immunology
Atherosclerosis
/ immunology
B-Lymphocytes, Regulatory
/ immunology
Cell Differentiation
Cells, Cultured
Cholesterol, Dietary
Diet, High-Fat
Disease Models, Animal
Lymphangiogenesis
Mice, Inbred C57BL
Mice, Knockout, ApoE
Phenotype
Plaque, Atherosclerotic
T Follicular Helper Cells
/ immunology
Atherosclerosis
Follicular helper T cell (TFH)
Follicular regulatory helper T cells (TFR)
Lymphangiogenesis
Regulatory B cell
Journal
Cardiovascular research
ISSN: 1755-3245
Titre abrégé: Cardiovasc Res
Pays: England
ID NLM: 0077427
Informations de publication
Date de publication:
22 02 2021
22 02 2021
Historique:
received:
25
01
2019
revised:
14
10
2019
accepted:
23
03
2020
pubmed:
29
3
2020
medline:
5
1
2022
entrez:
29
3
2020
Statut:
ppublish
Résumé
B cell functions in the process of atherogenesis have been investigated but several aspects remain to be clarified. In this study, we show that follicular regulatory helper T cells (TFR) control regulatory B cell (BREG) populations in Apoe-/- mice models on a high-cholesterol diet (HCD). Feeding mice with HCD resulted in up-regulation of TFR and BREG cell populations, causing the suppression of proatherogenic follicular helper T cell (TFH) response. TFH cell modulation is correlated with the growth of atherosclerotic plaque size in thoracoabdominal aortas and aortic root plaques, suggesting that TFR cells are atheroprotective. During adoptive transfer experiments, TFR cells transferred into HCD mice decreased TFH cell populations, atherosclerotic plaque size, while BREG cell population and lymphangiogenesis are significantly increased. Our results demonstrate that, through different strategies, both TFR and TFH cells modulate anti- and pro-atherosclerotic immune processes in an Apoe-/- mice model since TFR cells are able to regulate both TFH and BREG cell populations as well as lymphangiogenesis and lipoprotein metabolism.
Identifiants
pubmed: 32219371
pii: 5812780
doi: 10.1093/cvr/cvaa069
pmc: PMC7898950
doi:
Substances chimiques
Cholesterol, Dietary
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
743-755Commentaires et corrections
Type : CommentIn
Informations de copyright
© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology.
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