The cellular and signaling networks linking the immune system and metabolism in disease
Abstract
It is now recognized that obesity is driving the type 2 diabetes epidemic in Western countries. Obesity-associated chronic tissue inflammation is a key contributing factor to type 2 diabetes and cardiovascular disease, and a number of studies have clearly demonstrated that the immune system and metabolism are highly integrated. Recent advances in deciphering the various cellular and signaling networks that participate in linking the immune and metabolic systems together have contributed to understanding of the pathogenesis of metabolic diseases and may also inform new therapeutic strategies based on immunomodulation. Here we discuss how these various networks underlie the etiology of the inflammatory component of insulin resistance, with a particular focus on the central roles of macrophages in adipose tissue and liver.
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In obesity, the immune cell profile in adipose tissue is substantially altered, with accumulation of proinflammatory macrophages, neutrophils, and CD8+ T lymphocytes, and reduction of regulatory and eosinophilic T cells.
“In obesity, the immune cell profile in AT is substantially altered, for example, there is an accumulation of proinflammatory macrophages, neutrophils, and CD8+ T lymphocytes, while regulatory and eosinophilic T cells are substantially reduced.”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Osborn and Olefsky, 2012
This altered immune cell profile in adipose tissue contributes to inflammation that culminates in the development of systemic insulin resistance.
“This process contributes to inflammation that culminates in the development of systemic insulin resistance (Osborn and Olefsky, 2012; Mraz and Haluzik, 2014).”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Osborn and Olefsky, 2012
Adipocytes secrete TNF-α, IL-6, IL-12, IL-1β, and MCP-1 in large amounts.
“Osborn et al. [31] reported that adipocytes secrete TNF-α, IL-6, IL-12, IL-1β, and monocyte chemotactic protein-1(MCP-1) in large amounts.”
From The influence of obesity on the effects of spirulina supplementation in the human metabolic response of Korean elderly (2016) · cites this paper as [31]
Obesity is associated with systemic inflammation and impaired immunity.
“Obesity is associated with systemic inflammation and impaired immunity.”
From The influence of obesity on the effects of spirulina supplementation in the human metabolic response of Korean elderly (2016) · cites this paper as [31]
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- Authors
- Osborn, O., & Olefsky, J. M.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Olefsky, Jerrold M
- Venue
- Nature Medicine
- Published
- 2012-03
- Volume
- 18
- Issue
- 3
- Pages
- 363-374
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W1966336914
- Cited by
- 1,551
- References
- 169
- Citations by year
- 2026: 40 · 2025: 65 · 2024: 83 · 2023: 69 · 2022: 96 · 2021: 97 · 2020: 130 · 2019: 125 · 2018: 125 · 2017: 132 · 2016: 131 · 2015: 141 · 2014: 136 · 2013: 135 · 2012: 42
- FWCI
- 18.11
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- immunometabolism, obesity, type 2 diabetes, insulin resistance, chronic inflammation, macrophages, adipose tissue, liver, immunomodulation, metabolic disorders, signaling networks
- MeSH terms
- Adipose Tissue, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Humans, Immune System, Inflammation, Insulin Resistance, Macrophages, Metabolic Diseases, Obesity, Signal Transduction, Metabolic Networks and Pathways
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