Rapid linkage of innate immunological signals to adaptive immunity by the brain-fat axis
Open accessAbstract
Innate immunological signals induced by pathogen- and/or damage-associated molecular patterns are essential for adaptive immune responses, but it is unclear if the brain has a role in this process. Here we found that while the abundance of tumor-necrosis factor (TNF) quickly increased in the brain of mice following bacterial infection, intra-brain delivery of TNF mimicked bacterial infection to rapidly increase the number of peripheral lymphocytes, especially in the spleen and fat. Studies of various mouse models revealed that hypothalamic responses to TNF were accountable for this increase in peripheral lymphocytes in response to bacterial infection. Finally, we found that hypothalamic induction of lipolysis mediated the brain's action in promoting this increase in the peripheral adaptive immune response. Thus, the brain-fat axis is important for rapid linkage of innate immunity to adaptive immunity.
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Sleep disturbances can increase allergic reactions and worsen tumor-related immune responses.
“For instance, sleep disturbances can increase allergic reactions and worsen tumor-related immune responses (138, 226, 289, 404), which indicates that patients with these diseases could profit from sleep improvements.”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [289]
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References 52 · Cited by 40
- Authors
- Kim, M. S., Yan, J., Wu, W., Zhang, G., Zhang, Y., & Cai, D.
- Affiliations
- Albert Einstein College of Medicine (US)
- Corresponding author
- Cai, Dongsheng
- Venue
- Nature Immunology
- Published
- 2015-04-06
- Volume
- 16
- Issue
- 5
- Pages
- 525-533
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC4564120
- OpenAlex
- W1996793235
- Cited by
- 40
- References
- 52
- Citations by year
- 2026: 4 · 2025: 1 · 2023: 1 · 2022: 3 · 2021: 4 · 2020: 4 · 2019: 3 · 2018: 6 · 2017: 7 · 2016: 4 · 2015: 3
- FWCI
- 3.56
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG031774)
- National Heart, Lung, and Blood Institute (R01HL113180)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK099136, R01DK078750, P30DK026687)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
- Keywords
- hypothalamus, TNF-α, innate immunity, adaptive immunity, lymphocyte activation, bacterial infection, lipolysis, adipose tissue, spleen, neuroimmune interactions
- MeSH terms
- Adipose Tissue, Animals, Cell Count, Cells, Cultured, Fatty Acids, Hypothalamus, Immunity, Innate, Lipolysis, Listeriosis, Male, Mice, Inbred C57BL, Tumor Necrosis Factor-alpha, CD4-Positive T-Lymphocytes, Mice, Knockout, CD8-Positive T-Lymphocytes, Receptors, Tumor Necrosis Factor, Type I, Mice, Adaptive Immunity
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