Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary-lung axis.
Solar ultraviolet B radiation promotes α-MSH secretion to attenuate the function of ILC2s via the pituitary-lung axis.
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太阳紫外线B辐射通过垂体-肺轴促进α-MSH分泌,从而减弱ILC2s的功能。
DOI:
10.1038/s41467-023-41319-1
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发表时间:
2023-09-12
影响因子:
16.6
通讯作者:
Sun, Bing
中科院分区:
文献类型:
--
作者:
Huang, Yuying;Zhu, Lin;Cheng, Shipeng;Dai, Ranran;Huang, Chunrong;Song, Yanyan;Peng, Bo;Li, Xuezhen;Wen, Jing;Gong, Yi;Hu, Yunqian;Qian, Ling;Zhu, Linyun;Zhang, Fengying;Yu, Li;Yi, Chunyan;Gu, Wangpeng;Ling, Zhiyang;Ma, Liyan;Tang, Wei;Peng, Li;Shi, Guochao;Zhang, Yaguang;Sun, Bing
The immunomodulatory effects of ultraviolet B (UVB) radiation in human diseases have been described. Whether type 2 lung inflammation is directly affected by solar ultraviolet (UV) radiation is not fully understood. Here, we show a possible negative correlation between solar UVB radiation and asthmatic inflammation in humans and mice. UVB exposure to the eyes induces hypothalamus-pituitary activation and α-melanocyte-stimulating hormone (α-MSH) accumulation in the serum to suppress allergic airway inflammation by targeting group 2 innate lymphoid cells (ILC2) through the MC5R receptor in mice. The α-MSH/MC5R interaction limits ILC2 function through attenuation of JAK/STAT and NF-κB signaling. Consistently, we observe that the plasma α-MSH concentration is negatively correlated with the number and function of ILC2s in the peripheral blood mononuclear cells (PBMC) of patients with asthma. We provide insights into how solar UVB radiation-driven neuroendocrine α-MSH restricts ILC2-mediated lung inflammation and offer a possible strategy for controlling allergic diseases. Allergic asthma is episodic and associated with seasonal changes which may have links with UV exposure levels. Here the authors propose a link between UVB exposure and ILC2 function through α-MSH released from the pituitary gland which accumulates in the serum and alters ILC2 function through the MC5R receptor.
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影响因子:
64.5
作者:
Cui, Rutao;Widlund, Hans R.;Fisher, David E.
通讯作者:
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影响因子:
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DOI:
10.1073/pnas.0701764104
发表时间:
2007-05-22
影响因子:
11.1
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通讯作者:
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作者:
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通讯作者:
Finlay-Jones, JJ