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
Sun, Bing
中科院分区:
综合性期刊1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

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紫外线B(UVB)辐射在人类疾病中的免疫调节作用已被描述。2型肺炎是否直接受到太阳紫外线(UV)辐射的影响还不完全清楚。在这里,我们显示了太阳UVB辐射和人类和小鼠哮喘炎症之间可能的负相关性。UVB暴露于眼睛可诱导小鼠下丘脑-垂体激活和血清中α-黑素细胞刺激激素(α-MSH)蓄积,通过MC 5 R受体靶向第2组先天淋巴细胞(ILC 2)抑制过敏性气道炎症。α-MSH/MC 5 R相互作用通过减弱JAK/STAT和NF-κB信号传导限制ILC 2功能。哮喘患者血浆α-MSH浓度与外周血单个核细胞(PBMC)ILC 2的数量和功能呈负相关。我们提供了太阳UVB辐射驱动的神经内分泌α-MSH如何限制ILC 2介导的肺部炎症的见解,并提供了控制过敏性疾病的可能策略。过敏性哮喘是间歇性的,并与季节性变化有关,这可能与紫外线暴露水平有关。在这里,作者提出UVB暴露和ILC 2功能之间的联系,通过脑垂体释放的α-MSH积累在血清中,并通过MC 5 R受体改变ILC 2功能。
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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