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Contributions of innate type 2 inflammation to adipose function
W Reid Bolus1, Alyssa H Hasty2,3
1Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville TN 37232.
Journal of Lipid Research
|June 13, 2018
Summary
Obesity disrupts adipose tissue (AT) homeostasis, causing inflammation. Understanding innate type 2 immune cells in AT offers new therapeutic targets for metabolic diseases.
Area of Science:
- Immunometabolism
- Adipose tissue biology
- Innate immunity
Background:
- Obesity is linked to adipose tissue (AT) inflammation and dysfunction.
- White AT inflammation is a key factor in obesity-related diseases.
- Existing research focuses on immunometabolism and AT inflammation.
Purpose of the Study:
- To review literature on innate type 2 inflammation in adipose tissue.
- To highlight ongoing research and areas of debate in AT physiology.
- To identify potential therapeutic targets for obesity-associated AT inflammation.
Main Methods:
- Literature review of existing studies on innate immunity in AT.
- Analysis of the role of immune cells (macrophages, eosinophils, ILC2s) in AT homeostasis.
- Synthesis of current understanding of AT inflammation and its regulation.
Main Results:
- Innate immune cells, including M2-like macrophages, eosinophils, and innate lymphoid type 2 cells, play roles in AT homeostasis.
- Reducing AT inflammation can improve insulin action.
- The precise triggers of AT inflammation are still under investigation.
Conclusions:
- Innate type 2 inflammation is integral to adipose tissue function and homeostasis.
- Further research into AT physiology and immune cell interactions is crucial.
- Leveraging mechanisms of lean AT homeostasis may provide therapeutic strategies for obesity.
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