Cannabinoid receptor 2 signal promotes type 2 immunity in the lung

Cell insight Pub Date : 2023-10-01 DOI:10.1016/j.cellin.2023.100124

Tingting Liu , Jiaqi Liu , Hongjie Chen , Xin Zhou , Wei Fu , Ying Cao , Jing Yang

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Abstract

Type 2 immunity in the lung protects against pathogenic infection and facilitates tissue repair, but its dysregulation may lead to severe human diseases. Notably, cannabis usage for medical or recreational purposes has increased globally. However, the potential impact of the cannabinoid signal on lung immunity is incompletely understood. Here, we report that cannabinoid receptor 2 (CB2) is highly expressed in group 2 innate lymphoid cells (ILC2s) of mouse and human lung tissues. Of importance, the CB2 signal enhances the IL-33-elicited immune response of ILC2s. In addition, the chemogenetic manipulation of inhibitory G proteins (Gi) downstream of CB2 produces a similarly promotive effect. Conversely, the genetic deletion of CB2 mitigates the IL-33-elicited type 2 immunity in the lung. Also, such ablation of the CB2 signal ameliorates papain-induced tissue inflammation. Together, these results have elucidated a critical aspect of the CB2 signal in lung immunity, implicating its potential involvement in pulmonary diseases.

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大麻酚受体2信号促进肺部的2型免疫。

肺部的2型免疫可以预防病原性感染并促进组织修复，但其失调可能导致严重的人类疾病。值得注意的是，全球范围内用于医疗或娱乐目的的大麻使用量有所增加。然而，大麻素信号对肺部免疫的潜在影响尚不完全清楚。在此，我们报道了大麻素受体2（CB2）在小鼠和人类肺组织的第2组先天性淋巴细胞（ILC2s）中高度表达。重要的是，CB2信号增强了IL-33引发的ILC2的免疫应答。此外，CB2下游抑制性G蛋白（Gi）的化学遗传学操作也产生了类似的促进作用。相反，CB2的基因缺失减轻了肺中IL-33引发的2型免疫。此外，CB2信号的这种消融改善木瓜蛋白酶诱导的组织炎症。总之，这些结果阐明了CB2信号在肺部免疫中的一个关键方面，暗示其可能参与肺部疾病。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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