Regulatory T Cell Metabolism in Atherosclerosis

Regulatory T cells (Tregs) are capable of suppressing excessive immune responses to prevent autoimmunity and chronic inflammation. Decreased numbers of Tregs and impaired suppressive function are associated with the progression of atherosclerosis, a chronic inflammatory disease of the arterial wall...

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Vydáno v:	Metabolites Ročník 10; číslo 7; s. 279
Hlavní autoři:	Baardman, Jeroen, Lutgens, Esther
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	Basel MDPI AG 08.07.2020 MDPI
Témata:	Acute coronary syndromes Antigens Apolipoproteins Apoptosis Arteriosclerosis Atherosclerosis Autoimmunity Cardiovascular disease Cardiovascular diseases Cell growth Cholesterol Collagen Cytokines Foxp3 Homeostasis immunometabolism Immunoregulation Inflammatory diseases Lymphocytes Lymphocytes T Metabolism Proteins Review T cells Transcription factors Tregs
ISSN:	2218-1989, 2218-1989
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Abstract	Regulatory T cells (Tregs) are capable of suppressing excessive immune responses to prevent autoimmunity and chronic inflammation. Decreased numbers of Tregs and impaired suppressive function are associated with the progression of atherosclerosis, a chronic inflammatory disease of the arterial wall and the leading cause of cardiovascular disease. Therefore, therapeutic strategies to improve Treg number or function could be beneficial to preventing atherosclerotic disease development. A growing body of evidence shows that intracellular metabolism of Tregs is a key regulator of their proliferation, suppressive function, and stability. Here we evaluate the role of Tregs in atherosclerosis, their metabolic regulation, and the links between their metabolism and atherosclerosis.
AbstractList	Regulatory T cells (Tregs) are capable of suppressing excessive immune responses to prevent autoimmunity and chronic inflammation. Decreased numbers of Tregs and impaired suppressive function are associated with the progression of atherosclerosis, a chronic inflammatory disease of the arterial wall and the leading cause of cardiovascular disease. Therefore, therapeutic strategies to improve Treg number or function could be beneficial to preventing atherosclerotic disease development. A growing body of evidence shows that intracellular metabolism of Tregs is a key regulator of their proliferation, suppressive function, and stability. Here we evaluate the role of Tregs in atherosclerosis, their metabolic regulation, and the links between their metabolism and atherosclerosis. Regulatory T cells (Tregs) are capable of suppressing excessive immune responses to prevent autoimmunity and chronic inflammation. Decreased numbers of Tregs and impaired suppressive function are associated with the progression of atherosclerosis, a chronic inflammatory disease of the arterial wall and the leading cause of cardiovascular disease. Therefore, therapeutic strategies to improve Treg number or function could be beneficial to preventing atherosclerotic disease development. A growing body of evidence shows that intracellular metabolism of Tregs is a key regulator of their proliferation, suppressive function, and stability. Here we evaluate the role of Tregs in atherosclerosis, their metabolic regulation, and the links between their metabolism and atherosclerosis.Regulatory T cells (Tregs) are capable of suppressing excessive immune responses to prevent autoimmunity and chronic inflammation. Decreased numbers of Tregs and impaired suppressive function are associated with the progression of atherosclerosis, a chronic inflammatory disease of the arterial wall and the leading cause of cardiovascular disease. Therefore, therapeutic strategies to improve Treg number or function could be beneficial to preventing atherosclerotic disease development. A growing body of evidence shows that intracellular metabolism of Tregs is a key regulator of their proliferation, suppressive function, and stability. Here we evaluate the role of Tregs in atherosclerosis, their metabolic regulation, and the links between their metabolism and atherosclerosis.
Author	Baardman, Jeroen Lutgens, Esther
AuthorAffiliation	1 Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; e.lutgens@amsterdamumc.nl 3 German Center for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, 80336 Munich, Germany 2 Institute for Cardiovascular Prevention (IPEK), Klinikum der Universität München (KUM), Ludwig-Maximilians-Universität (LMU) München, 80336 Munich, Germany
AuthorAffiliation_xml	– name: 2 Institute for Cardiovascular Prevention (IPEK), Klinikum der Universität München (KUM), Ludwig-Maximilians-Universität (LMU) München, 80336 Munich, Germany – name: 1 Department of Medical Biochemistry, Experimental Vascular Biology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; e.lutgens@amsterdamumc.nl – name: 3 German Center for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, 80336 Munich, Germany
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SubjectTerms	Acute coronary syndromes Antigens Apolipoproteins Apoptosis Arteriosclerosis Atherosclerosis Autoimmunity Cardiovascular disease Cardiovascular diseases Cell growth Cholesterol Collagen Cytokines Foxp3 Homeostasis immunometabolism Immunoregulation Inflammatory diseases Lymphocytes Lymphocytes T Metabolism Proteins Review T cells Transcription factors Tregs
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Title	Regulatory T Cell Metabolism in Atherosclerosis
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