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The role of infiltrating immune cells in dysfunctional adipose tissue

Adipose tissue (AT) dysfunction, characterized by loss of its homeostatic functions, is a hallmark of non-communicable diseases. It is characterized by chronic low-grade inflammation and is observed in obesity, metabolic disorders such as insulin resistance and diabetes. While classically it has bee...

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Autores principales: Guzik, Tomasz J., Skiba, Dominik S., Touyz, Rhian M., Harrison, David G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5852626/
https://www.ncbi.nlm.nih.gov/pubmed/28838042
http://dx.doi.org/10.1093/cvr/cvx108
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author Guzik, Tomasz J.
Skiba, Dominik S.
Touyz, Rhian M.
Harrison, David G.
author_facet Guzik, Tomasz J.
Skiba, Dominik S.
Touyz, Rhian M.
Harrison, David G.
author_sort Guzik, Tomasz J.
collection PubMed
description Adipose tissue (AT) dysfunction, characterized by loss of its homeostatic functions, is a hallmark of non-communicable diseases. It is characterized by chronic low-grade inflammation and is observed in obesity, metabolic disorders such as insulin resistance and diabetes. While classically it has been identified by increased cytokine or chemokine expression, such as increased MCP-1, RANTES, IL-6, interferon (IFN) gamma or TNFα, mechanistically, immune cell infiltration is a prominent feature of the dysfunctional AT. These immune cells include M1 and M2 macrophages, effector and memory T cells, IL-10 producing FoxP3+ T regulatory cells, natural killer and NKT cells and granulocytes. Immune composition varies, depending on the stage and the type of pathology. Infiltrating immune cells not only produce cytokines but also metalloproteinases, reactive oxygen species, and chemokines that participate in tissue remodelling, cell signalling, and regulation of immunity. The presence of inflammatory cells in AT affects adjacent tissues and organs. In blood vessels, perivascular AT inflammation leads to vascular remodelling, superoxide production, endothelial dysfunction with loss of nitric oxide (NO) bioavailability, contributing to vascular disease, atherosclerosis, and plaque instability. Dysfunctional AT also releases adipokines such as leptin, resistin, and visfatin that promote metabolic dysfunction, alter systemic homeostasis, sympathetic outflow, glucose handling, and insulin sensitivity. Anti-inflammatory and protective adiponectin is reduced. AT may also serve as an important reservoir and possible site of activation in autoimmune-mediated and inflammatory diseases. Thus, reciprocal regulation between immune cell infiltration and AT dysfunction is a promising future therapeutic target.
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spelling pubmed-58526262018-03-23 The role of infiltrating immune cells in dysfunctional adipose tissue Guzik, Tomasz J. Skiba, Dominik S. Touyz, Rhian M. Harrison, David G. Cardiovasc Res Invited Spotlight Reviews Adipose tissue (AT) dysfunction, characterized by loss of its homeostatic functions, is a hallmark of non-communicable diseases. It is characterized by chronic low-grade inflammation and is observed in obesity, metabolic disorders such as insulin resistance and diabetes. While classically it has been identified by increased cytokine or chemokine expression, such as increased MCP-1, RANTES, IL-6, interferon (IFN) gamma or TNFα, mechanistically, immune cell infiltration is a prominent feature of the dysfunctional AT. These immune cells include M1 and M2 macrophages, effector and memory T cells, IL-10 producing FoxP3+ T regulatory cells, natural killer and NKT cells and granulocytes. Immune composition varies, depending on the stage and the type of pathology. Infiltrating immune cells not only produce cytokines but also metalloproteinases, reactive oxygen species, and chemokines that participate in tissue remodelling, cell signalling, and regulation of immunity. The presence of inflammatory cells in AT affects adjacent tissues and organs. In blood vessels, perivascular AT inflammation leads to vascular remodelling, superoxide production, endothelial dysfunction with loss of nitric oxide (NO) bioavailability, contributing to vascular disease, atherosclerosis, and plaque instability. Dysfunctional AT also releases adipokines such as leptin, resistin, and visfatin that promote metabolic dysfunction, alter systemic homeostasis, sympathetic outflow, glucose handling, and insulin sensitivity. Anti-inflammatory and protective adiponectin is reduced. AT may also serve as an important reservoir and possible site of activation in autoimmune-mediated and inflammatory diseases. Thus, reciprocal regulation between immune cell infiltration and AT dysfunction is a promising future therapeutic target. Oxford University Press 2017-07 2017-07-11 /pmc/articles/PMC5852626/ /pubmed/28838042 http://dx.doi.org/10.1093/cvr/cvx108 Text en © The Author. Published on behalf of the European Society of Cardiology http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Invited Spotlight Reviews
Guzik, Tomasz J.
Skiba, Dominik S.
Touyz, Rhian M.
Harrison, David G.
The role of infiltrating immune cells in dysfunctional adipose tissue
title The role of infiltrating immune cells in dysfunctional adipose tissue
title_full The role of infiltrating immune cells in dysfunctional adipose tissue
title_fullStr The role of infiltrating immune cells in dysfunctional adipose tissue
title_full_unstemmed The role of infiltrating immune cells in dysfunctional adipose tissue
title_short The role of infiltrating immune cells in dysfunctional adipose tissue
title_sort role of infiltrating immune cells in dysfunctional adipose tissue
topic Invited Spotlight Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5852626/
https://www.ncbi.nlm.nih.gov/pubmed/28838042
http://dx.doi.org/10.1093/cvr/cvx108
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