Autocrine motility factor receptor as a therapeutic target for asthma: comments on 'AMFR drives allergic asthma development by promoting alveolar macrophage-derived GM-CSF production'.
Autocrine motility factor receptor as a therapeutic target for asthma: comments on 'AMFR drives allergic asthma development by promoting alveolar macrophage-derived GM-CSF production'.
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DOI：
10.1093/jmcb/mjac032
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发表时间：
2022-08-26
影响因子：
5.5
通讯作者：
中科院分区：
文献类型：
--
作者：
哮喘是一种以气道高反应性和组织重塑为特征的慢性炎症性疾病（Nobs et al., 2021）。虽然对哮喘发病机制的探索越来越多，但哮喘的潜在分子和细胞机制尚不清楚，现有的靶向治疗策略仍然有限且无效。因此，有必要探索哮喘的发病机制，寻找哮喘治疗的新靶点。肺泡巨噬细胞（Alveolar macrophages, AMs）是肺中重要的免疫系统细胞之一，与哮喘的发生和发展有关（Evren et al., 2020）。越来越多的证据表明，AMs可以促进T辅助2 （Th2）细胞的分化和增殖，介导炎症部位嗜酸性粒细胞的募集、积累和脱颗粒，并调节上皮完整性和平滑肌反应（Evren et al., 2020）。然而，关于AMs在哮喘发病机制中的作用，其调控细胞间串扰的详细机制仍然是一个知识空白。
Asthma is a chronic inflammatory disease characterized by airway hyper-responsiveness and tissue remodeling (Nobs et al., 2021). Although explorations into the pathogenesis of asthma are increasing, the underlying molecular and cellular mechanisms of asthma remain indistinct, and existing targeted therapy strategies are still limited and ineffective. Therefore, it is necessary to explore the mechanisms of asthma and identify new therapeutic targets for asthma treatment. Alveolar macrophages (AMs), one of the prominent immune system cells in the lung, have been implicated in the development and progression of asthma (Evren et al., 2020). Accumulating evidence suggests that AMs can promote the differentiation and proliferation of T helper 2 (Th2) cells, mediate the recruitment, accumulation, and degranulation of eosinophils within inflamed sites, and regulate epithelial integrity and smooth muscle responses (Evren et al., 2020). However, the detailed mechanism by which AMs regulate cell–cell crosstalk in asthma is still a knowledge gap regarding the roles of AMs in asthma pathogenesis.
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影响因子：
10
作者：
Saha, S.;Doe, C.;Brightling, C. E.
通讯作者：
Brightling, C. E.
DOI：
10.1084/jem.20210745
发表时间：
2021-10-04
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Gschwend J;Sherman SPM;Ridder F;Feng X;Liang HE;Locksley RM;Becher B;Schneider C
通讯作者：
Schneider C
影响因子：
30.5
作者：
Delconte, Rebecca B.;Kolesnik, Tatiana B.;Huntington, Nicholas D.
通讯作者：
Huntington, Nicholas D.
影响因子：
14.2
作者：
Nobs, Samuel Philip;Pohlmeier, Lea;Kopf, Manfred
通讯作者：
Kopf, Manfred
E3 泛素连接酶 AMFR 和 INSIG1 通过修改适配器 STING 桥接 TBK1 激酶的激活
影响因子：
32.4
作者：
Wang, Qiang;Liu, Xing;Wang, Chen
通讯作者：
Wang, Chen