Dectin-2的作用(基因符号，Clec4n)在屋尘螨(HDM)中诱导Th2免疫应答的确切机制仍存在争议。在这项研究中,我们说明了这一点，Clec4n-/-小鼠在HDM攻击后Th2免疫应答降低，这可能归因于Clec4n-/-小鼠肺中2型常规树突状细胞（cDC2s）的显着减少，因为挑战后来自Clec4n-/-小鼠的肺的cDC2s诱导Th2应答的能力较低,IL-4/IL-13的产生减少。进一步的体外实验表明，HDM刺激后，Clec4n-/-BMDCs的激活显着降低，同时Syk-NF-κB和Syk-JNK信号通路的激活降低。重要的是,哮喘患者PBMC中Dectin-2的表达明显高于健康对照组。一起来看,这些结果表明Dectin-2可以促进肺cDC2s的激活，它极化了Th2免疫反应，概述了哮喘发展的新机制。
The role of Dectin-2 (gene symbol, Clec4n) in house dust mite (HDM) induced Th2 immune response and the exact mechanism remains controversial. In this study, we illustrated that, Clec4n-/- mice had decreased Th2 immune response following HDM challenge, which may ascribe to dramatically reduced type 2 conventional dendritic cells (
cDC2s) in lung of Clec4n-/- mice, as
cDC2s from lung of Clec4n-/- mice after challenging had less ability to induce Th2 response with decreased production of IL-4/IL-13. Further in vitro experiments showed the activation of Clec4n-/--BMDCs significantly decreased after HDM stimulation accompanied with decreased activation of Syk-NF-κB and Syk-JNK signal pathway. Importantly, Dectin-2 expression in PBMCs from asthmatic patients was significantly higher than that in healthy controls. Taken together, these results demonstrated that Dectin-2 could promote
cDC2s activation in lung, which polarizes Th2 immune response outlining a novel mechanism of asthma development.
