免疫系统
免疫学
慢性阻塞性肺病
主要组织相容性复合体
关贸总协定3
树突状细胞
抗原
生物
抗原呈递
获得性免疫系统
医学
T细胞
转录因子
基因
内科学
遗传学
作者
Fang He,Nian Wang,Xiaoyuan Yu,Yufan Zheng,Qun Li,Qingzi Chen,Jinding Pu,Naijian Li,Weifeng Zou,Bing Li,Pixin Ran
标识
DOI:10.1016/j.jhazmat.2022.129459
摘要
Chronic obstructive pulmonary disease (COPD) is a heterogeneous illness associated with aberrant inflammatory immune reaction in the lung in response to noxious particles and gases. Our previous epidemiological studies discovered that long-term exposure to air pollution PM was associated with an increase in the incidence of COPD and lung function decline, but the impact of air pollution on the onset of COPD and its pathogenesis remains obscure. In recent years, long noncoding RNAs (lncRNAs) have been documented to have a crucial role in COPD. Our preliminary study found that the expression of lncRNA MHC-R in the lung tissues of rats exposed to air pollution PM was dramatically elevated, and the specific expression was mainly focused on the immune-related MHC I, antigen-presenting, and adaptive immune response. After transcription factor prediction, it was found that GATA3 could be combined with the specific sequence of the lncRNA MHC-R promoter region. Dendritic cells (DCs) are necessary antigen-presenting cells (APCs) with the most potent antigen-presenting function. We proved that GATA3/lncRNA MHC-R might regulate the immune activities of DCs to participate in the pathogenic mechanism of COPD induced by air pollution PM, which opens up a new way for early COPD diagnosis and treatment.
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