Altered Tregs Differentiation and Impaired Autophagy Correlate to Atherosclerotic Disease.


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2020
Historique:
received: 11 10 2019
accepted: 13 02 2020
entrez: 2 4 2020
pubmed: 2 4 2020
medline: 2 3 2021
Statut: epublish

Résumé

Atherosclerosis is a progressive vascular disease representing the primary cause of morbidity and mortality in developed countries. Formerly, atherosclerosis was considered as a mere passive accumulation of lipids in blood vessels. However, it is now clear that atherosclerosis is a complex and multifactorial disease, in which the involvement of immune cells and inflammation play a key role. A variety of studies have shown that autophagy-a cellular catalytic mechanism able to remove injured cytoplasmic components in response to cellular stress-may be proatherogenic. So far, in this context, its role has been investigated in smooth muscle cells, macrophages, and endothelial cells, while the function of this catabolic protective process in lymphocyte functionality has been overlooked. The few studies carried out so far, however, suggested that autophagy modulation in lymphocyte subsets may be functionally related to plaque formation and development. Therefore, in this research, we aimed at better clarifying the role of lymphocyte subsets, mainly regulatory T cells (Tregs), in human atherosclerotic plaques and in animal models of atherosclerosis investigating the contribution of autophagy on immune cell homeostasis. Here, we investigate basal autophagy in a mouse model of atherosclerosis, apolipoprotein E (ApoE)-knockout (KO) mice, and we analyze the role of autophagy in driving Tregs polarization. We observed defective maturation of Tregs from ApoE-KO mice in response to tumor growth factor-β (TGFβ). TGFβ is a well-known autophagy inducer, and Tregs maturation defects in ApoE-KO mice seem to be related to autophagy impairment. In this work, we propose that autophagy underlies Tregs maturation, advocating that the study of this process in atherosclerosis may open new therapeutic strategies.

Identifiants

pubmed: 32231663
doi: 10.3389/fimmu.2020.00350
pmc: PMC7082762
doi:

Substances chimiques

Apolipoproteins E 0
FOXP3 protein, human 0
Forkhead Transcription Factors 0
Transforming Growth Factor beta 0
Aldosterone 4964P6T9RB

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

350

Informations de copyright

Copyright © 2020 Mandatori, Pacella, Marzolla, Mammi, Starace, Padula, Vitiello, Armani, Savoia, Taurino, De Zio, Giampietri, Piconese, Cecconi, Caprio and Filippini.

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Auteurs

Sara Mandatori (S)

Unit of Histology and Medical Embryology, Department of Anatomy, Histology, Forensic Medicine and Orthopaedics, Sapienza University of Rome, Rome, Italy.

Ilenia Pacella (I)

Laboratory of Cellular and Molecular Immunology, Department of Internal Clinical Sciences, Anaesthesiology and Cardiovascular Sciences, Sapienza Università di Roma, Rome, Italy.
Laboratory Affiliated to Istituto Pasteur Italia - Fondazione Cenci Bolognetti, Rome, Italy.

Vincenzo Marzolla (V)

Laboratory of Cardiovascular Endocrinology, IRCCS San Raffaele Pisana, Rome, Italy.

Caterina Mammi (C)

Laboratory of Cardiovascular Endocrinology, IRCCS San Raffaele Pisana, Rome, Italy.

Donatella Starace (D)

UOC, Clinical Pathology, San Giovanni Addolorata Hospital, Rome, Italy.

Fabrizio Padula (F)

Unit of Histology and Medical Embryology, Department of Anatomy, Histology, Forensic Medicine and Orthopaedics, Sapienza University of Rome, Rome, Italy.

Laura Vitiello (L)

Flow Cytometry Unit, IRCCS San Raffaele Pisana, Rome, Italy.

Andrea Armani (A)

Laboratory of Cardiovascular Endocrinology, IRCCS San Raffaele Pisana, Rome, Italy.

Carmine Savoia (C)

Cardiology Unit, Department of Clinical and Molecular Medicine, Sant'Andrea Hospital, Sapienza University of Rome, Rome, Italy.

Maurizio Taurino (M)

Unit of Vascular Surgery, Department of Clinical and Molecular Medicine, Sant'Andrea Hospital, Sapienza University of Rome, Rome, Italy.

Daniela De Zio (D)

Cell Stress and Survival Unit, Center of Autophagy, Recycling and Disease (CARD), Danish Cancer Society Research Center, Copenhagen, Denmark.

Claudia Giampietri (C)

Unit of Human Anatomy, Department of Anatomy, Histology, Forensic Medicine and Orthopaedics, Sapienza University of Rome, Rome, Italy.

Silvia Piconese (S)

Laboratory of Cellular and Molecular Immunology, Department of Internal Clinical Sciences, Anaesthesiology and Cardiovascular Sciences, Sapienza Università di Roma, Rome, Italy.
Laboratory Affiliated to Istituto Pasteur Italia - Fondazione Cenci Bolognetti, Rome, Italy.

Francesco Cecconi (F)

Cell Stress and Survival Unit, Center of Autophagy, Recycling and Disease (CARD), Danish Cancer Society Research Center, Copenhagen, Denmark.
Department of Paediatric Haematology and Oncology, IRCCS Bambino Gesù Children's Hospital, Rome, Italy.
Department of Biology, University of Rome Tor Vergata, Rome, Italy.

Massimiliano Caprio (M)

Laboratory of Cardiovascular Endocrinology, IRCCS San Raffaele Pisana, Rome, Italy.
Department of Human Sciences and Promotion of the Quality of Life, San Raffaele Roma Open University, Rome, Italy.

Antonio Filippini (A)

Unit of Histology and Medical Embryology, Department of Anatomy, Histology, Forensic Medicine and Orthopaedics, Sapienza University of Rome, Rome, Italy.

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