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Neuroimmunometabolism in Health and Disease
Charles A P Sweeney1, Hanyu Liu1, Matthew Dean1
1Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom;
Annual Review of Immunology
|February 5, 2026
Summary
Sympathetic neurons control body weight by regulating adipose tissue. Obesity disrupts this neuroimmune communication, worsening weight gain and potentially linking obesity to cancer via shared signaling pathways.
Area of Science:
- Neuroscience
- Immunology
- Metabolism
Background:
- Sympathetic neurons regulate adipose tissue function and body weight.
- Neuroimmune crosstalk is crucial for maintaining metabolic homeostasis.
- Obesity is associated with neuroinflammation and impaired sympathetic signaling.
Purpose of the Study:
- To review the neuroimmune mechanisms of sympathetic neuron regulation of adipose tissue.
- To explore the role of neuroinflammation in obesity-associated weight gain.
- To examine shared neuroimmune and immunometabolic pathways in obesity and cancer.
Main Methods:
- Literature review of neuroimmune and immunometabolic mechanisms.
- Analysis of sympathetic-adipose communication under healthy and obese conditions.
- Examination of the link between obesity, cancer, and neuroimmunometabolic signaling.
Main Results:
- Healthy sympathetic-adipose communication relies on anti-inflammatory cues and neurotrophic factors.
- Obesity weakens the sympathetic perineurial barrier, leading to neuroinflammation and neuropathy.
- Impaired neuroimmune signaling in obesity may contribute to shared mechanisms with cancer.
Conclusions:
- Sympathetic neuropathy and neuroinflammation exacerbate weight gain in obesity.
- Neuropeptide Y and tachykinins from sympathetic neurons are vital for brown adipose tissue thermogenesis.
- Dysfunctional neuroimmunometabolic signaling may underlie the obesity-cancer link.
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