期刊
IMMUNITY
卷 54, 期 6, 页码 1219-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2021.03.025
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资金
- National Health and Medical Research Council of Australia [1082450, 1161734, 1154457, 1147498]
- Australian Research Council [CE140100011]
- National Health and Medical Research Council of Australia [1161734, 1082450, 1154457] Funding Source: NHMRC
The study demonstrates that adrenergic receptors play a crucial role in modulating leukocyte mobility and immune responses, shedding light on the link between sympathetic nervous system activation and compromised immunity.
The sympathetic nervous system (SNS) controls various physiological functions via the neurotransmitter noradrenaline. Activation of the SNS in response to psychological or physical stress is frequently associated with weakened immunity. Here, we investigated how adrenoceptor signaling influences leukocyte behavior. Intravital two-photon imaging after injection of noradrenaline revealed transient inhibition of CD8(+) and CD4(+) T cell locomotion in tissues. Expression of beta-adrenergic receptor in hematopoietic cells was not required for NA-mediated inhibition of motility. Rather, chemogenetic activation of the SNS or treatment with adrenergic receptor agonists induced vasoconstriction and decreased local blood flow, resulting in abrupt hypoxia that triggered rapid calciumsignaling in leukocytes and halted cellmotility. Oxygen supplementation reversed these effects. Treatmentwith adrenergic receptor agonists impaired T cell responses induced in response to viral and parasitic infections, as well as anti-tumor responses. Thus, stimulation of the SNS impairs leukocyte mobility, providing a mechanistic understanding of the link between adrenergic receptors and compromised immunity.
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