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Review
. 2015 Mar;23(3):512-8.
doi: 10.1002/oby.21003. Epub 2015 Jan 22.

Adipose tissue as an immunological organ

Affiliations
Review

Adipose tissue as an immunological organ

Ryan W Grant et al. Obesity (Silver Spring). 2015 Mar.

Abstract

Objective: This review will focus on the immunological aspects of adipose tissue and its potential role in development of chronic inflammation that instigates obesity-associated comorbidities.

Methods: The review used PubMed searches of current literature to examine adipose tissue leukocytosis.

Results and conclusions: The adipose tissue of obese subjects becomes inflamed and contributes to the development of insulin resistance, type 2 diabetes, and metabolic syndrome. Numerous immune cells including B cells, T cells, macrophages, and neutrophils have been identified in adipose tissue, and obesity influences both the quantity and the nature of immune cell subtypes, which emerges as an active immunological organ capable of modifying whole-body metabolism through paracrine and endocrine mechanisms. Adipose tissue is a large immunologically active organ during obesity and displays hallmarks of both and innate and adaptive immune response. Despite the presence of hematopoietic lineage cells in adipose tissue, it is unclear whether the adipose compartment has a direct role in immune surveillance or host defense. Understanding the interactions between leukocytes and adipocytes may reveal the clinically relevant pathways that control adipose tissue inflammation and is likely to reveal mechanisms by which obesity contributes to increased susceptibility to both metabolic and certain infectious diseases.

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Conflict of interest statement

Conflicts of interest: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Generation of inflammation in adipose tissue. Adipocyte death releases cytosolic constituents and exposes the lipid droplet. Macrophages engulf or are activated by adipocyte constituents leading to macrophage production of cytokines. B cells are also activated leading to the production of antibodies and MHCII dependent T cell interaction which may contribute to insulin resistance. IL-1β secreted by macrophages and antigen presentation drives the clonal expansion of T cells and shifts the balance of T cells in adipose tissue from naïve to effector memory cells. Dashed lines indicate possible interactions between cells.

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MeSH terms

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