Gateway reflex: neural activation-mediated immune cell gateways in the central nervous system
Abstract
The neural regulation of organs can be categorized as systemic or local. Whereas systemic regulation by the hypothalamus–pituitary–adrenal gland-mediated release of steroid hormones has been well studied, the mechanisms for local regulation have only recently emerged. Two types of local neural regulation are known, the gateway reflex and the inflammatory reflex. The gateway reflex describes a mechanism that converts regional neural stimulations into inflammatory outputs by changing the state of specific blood vessels. Molecularly, the enhancement of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity in endothelial cells by neurotransmitters, such as noradrenaline and ATP, induces an enhanced production of pro-inflammatory mediators, including chemokines, which form immune cell gateways at specific vessels. Several types of gateway reflex have been identified, and each regulates distinct organs by creating gateways for autoreactive T cells that induce local inflammation. On the other hand, the inflammatory reflex elicits an anti-inflammatory response through vagal nerves. Here, we summarize recent works on these two local neuro-immune interactions, giving special focus to the gateway reflex.
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The gateway reflex activates the IL-6 Amp through beta-adrenergic receptors in the dorsal vessels of the fifth lumbar cord, allowing for autoreactive T-cell accumulation and disease onset.
“This neural pathway, which is now called the gateway reflex (286, 287), activates the IL-6 Amp through beta-adrenergic receptors in the dorsal vessels of the fifth lumbar cord, allowing for autoreactive T-cell accumulation and disease onset (54).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [286]
The Fig. 1 caption and “Gravity is a positive regulator of local inflammation” section describe norepinephrine enhancing the inflammation amplifier at L5 dorsal vessels, recruiting pathogenic CD4+ T cells in a preclinical EAE mouse model. The section also reports that blocking adrenergic receptors reduced chemokine expression and EAE severity, but it does not specify beta-adrenergic receptors for this pathway. The claim’s receptor subtype is therefore not established by this copy. (LLM, conf=0.85)
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Self-citationUchida, M., Yamamoto, R., Matsuyama, S., Murakami, K., Hasebe, R., Hojyo, S., Tanaka, Y., & Murakami, M. (2021) · International Immunology · doi:10.1093/intimm/dxab022 · Cited by 9 · see citing works
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Goldstein, D. S., & Benarroch, E. E. (2023) · Elsevier eBooks · doi:10.1016/b978-0-12-820480-1.00023-1
- Authors
- Kamimura, D., Ohki, T., Arima, Y., & Murakami, M.
- Affiliations
- Hokkaido University (JP)
- Corresponding author
- Murakami, Masaaki
- Venue
- International Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2018-05-15
- Volume
- 30
- Issue
- 7
- Pages
- 281-289
- ISSN
- 0953-8178 (ISSN-L)
- 1460-2377
- OpenAlex
- W2806467491
- Cited by
- 12
- References
- 94
- Citations by year
- 2024: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 5 · 2018: 1
- FWCI
- 0.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- KAKENHI
- Takeda Science Foundation
- Institute for Fermentation Osaka
- Mitsubishi Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Suzuken Memorial Foundation
- Japan Prize Foundation
- Ono Medical Research Foundation
- Kanzawa Medical Research Foundation
- Kishimoto Foundation
- Nagao Takeshi Research Foundation
- Japan Multiple Sclerosis Society
- Kanae Fundation
- Tokyo Medical Research Foundation
- Topics
- Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Keywords
- cholinergic anti-inflammatory pathway, neuroimmune interactions, NF-κB, endothelial cells, norepinephrine, ATP, chemokines, autoreactive T cells, vagus nerve, anti-inflammatory response, pro-inflammatory mediators
- MeSH terms
- Animals, Central Nervous System, Humans, Lymphocytes, Neurons
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