Adipose tissue as an immunological organ
Open accessAbstract
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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These events induce secretion of pro-inflammatory molecules by adipocytes, endothelial cells, and adipose immune cells, leading to infiltration of immune cells and a reduction in T regulatory cells, amplifying inflammation that can become prolonged and systemic.
“These events can induce the secretion of numerous pro-inflammatory molecules, including adipokines, cytokines (for example, IL-1β, IL-6, TNF-α), and chemokines (especially monocyte chemoattractant protein-1) by adipocytes, endothelial cells and resident adipose tissue immune cells (for example, macrophages)105–108. This in turn leads to the infiltration of various immune cells in the VAT,”
From Chronic inflammation in the etiology of disease across the life span (2019) · cites this paper as [109]
In T2DM and obesity, the adipocytes of expanded EAT release large amounts of FAs that trigger macrophage infiltration and secretion of pro-inflammatory adipocytokines including leptin, TNF-α, IL-6, IL-1b and resistin; simultaneously, the production of adiponectin diminishes.
“In T2DM and obesity, the adipocytes of expanded EAT release large amounts of FAs that trigger macrophage infiltration and secretion of pro-inflammatory adipocytokines including leptin, TNF-α, IL-6, IL-1b and resistin. Simultaneously, the production of adiponectin diminishes [18,91].”
From Dysregulated epicardial adipose tissue as a risk factor and potential therapeutic target of heart failure with preserved ejection fraction in diabetes (2022) · cites this paper as [91]
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Obesogenic Memory Maintains Adipose Tissue Inflammation and Insulin Resistance
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Specific Strains of Lactic Acid Bacteria Differentially Modulate the Profile of Adipokines In Vitro
Fabersani, E., Mukdsi, M. C. A., Ross, R., Medina, R. B., González, S., & Gauffin-Cano, P. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.00266 · Cited by 44 · see citing works
- Authors
- Grant, R. W., & Dixit, V. D.
- Affiliations
- Purdue University West Lafayette (US)
- Yale University (US)
- Corresponding author
- Grant, Ryan W.
- Venue
- Obesity
- Publisher
- Wiley
- Published
- 2015-01-22
- Volume
- 23
- Issue
- 3
- Pages
- 512-518
- ISSN
- 1930-7381 (ISSN-L)
- 1930-739X
- PMC
- PMC4340740
- OpenAlex
- W2108102649
- Cited by
- 453
- References
- 79
- Citations by year
- 2026: 25 · 2025: 30 · 2024: 42 · 2023: 35 · 2022: 31 · 2021: 60 · 2020: 51 · 2019: 46 · 2018: 36 · 2017: 36 · 2016: 32 · 2015: 26 · 2013: 2
- FWCI
- 5.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Obesity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (DK090556)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- adipose tissue, adipose tissue inflammation, chronic inflammation, macrophages, neutrophils, B cells, T cells, insulin resistance, type 2 diabetes, metabolic syndrome, paracrine signaling, hormone signaling, adipocytes, innate and adaptive immunity, obesity-related comorbidities
- MeSH terms
- Adipose Tissue, Diabetes Mellitus, Type 2, Humans, Immunity, Innate, Inflammation, Obesity, Metabolic Syndrome, Adaptive Immunity
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