展开图
肺炎
转录组
生物
免疫系统
计算生物学
地图集(解剖学)
免疫学
医学
病理
计算机科学
遗传学
人工智能
内科学
基因
基因表达
解剖
作者
Kun Xiao,Yan Cao,Zhihai Han,Yuxiang Zhang,Laurence Don Wai Luu,Liang Chen,Peng Yan,Wei Chen,Jiaxing Wang,Ying Liang,Xin Shi,Xiuli Wang,Fan Wang,Ye Hu,Zhengjun Wen,Yong Chen,Yuwei Yang,Haotian Yu,Lixin Xie,Yi Wang
标识
DOI:10.1038/s41392-024-02093-8
摘要
T cell function, potentially reflecting a compensatory mechanism. Dysregulated neutrophil and macrophage responses contributed significantly to the pathogenesis of severe disease. Immature neutrophils promote excessive inflammation and suppress T cell activation, while a specific macrophage subset (Macro_03_M1) displaying features akin to myeloid-derived suppressor cells (M-MDSCs) suppress T cells and promote inflammation. Together, these findings highlight potential therapeutic targets for modulating immune responses and improving clinical outcomes in bacterial pneumonia.
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