| 项目编号 |
PRJCA035327 |
| 项目标题 |
The nuclear factor ID3 promotes antibacterial innate immunity in macrophages through ZBP1 |
| 涉及领域 |
Medical |
| 数据类型 |
Transcriptome or Gene expression
ChIP-seq
|
| 物种名称 |
Mus musculus
|
| 描述信息 |
Macrophages are central mediators of anti-bacterial innate immunity and the regulation of innate immune responses requires the timely orchestration of transcription factors and epigenetic modifications. Inhibitor of differentiation 3 (ID3) has been found to determine the differentiation and function of multiple immune cells. However, the role and regulatory mechanism of ID3 in macrophages during pathogen infection remain unclear. Here we show that bacterial infection significantly reduces the acetylation of histone H2BK16, which in turn downregulates the expression of ID3. Loss- and gain-of-function experiments demonstrate that ID3 confers potent antibacterial activity to macrophages. Mechanistically, deficiency of ID3 attenuates the inflammatory and antimicrobial immune response of macrophages, specially inhibits the Z-form nucleic acid-binding protein-1 (ZBP1) expression through the binding of the transcription factor E2A at the ZBP1 locus, which further dampens the NLRP3 inflammasome activation. In vivo experiments demonstrate the potential of H2BK16ac and ID3 as antibacterial targets. These findings unveil infection-driven histone modification governing the ID3 expression and macrophage activation, with implications for epigenetic- and transcriptional- based infectious disease therapies. |
| 样品范围 |
Monoisolate |
| 发布日期 |
2025-01-20 |
| 项目资金来源 |
| 机构 |
项目类型 |
授权项目ID |
授权项目名称 |
| National Natural Science Foundation of China (NSFC)
|
General Program
|
82472285
|
|
| National Natural Science Foundation of China (NSFC)
|
General Program
|
81830068
|
|
| National Natural Science Foundation of China (NSFC)
|
General Program
|
82272351
|
|
|
|
| 提交者 |
Wanqiu
Huang (wanqiuhuang@126.com)
|
| 提交单位 |
Shanghai Jiao Tong University School of Medicine |
| 提交日期 |
2025-01-20 |
