在Toxoplasma gondii感染期间,LILRB4通过SHP-2/STAT6通路调节了落叶MDSC的功能
Yuantao Li1, Jingjing Guo1, Haixia Zhang2
1Department of Gynecology and Obstetrics, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, Shandong, People's Republic of China.
Parasites & vectors
|July 17, 2023
概括
毒素菌感染降低了LILRB4表达在状骨髓衍生抑制细胞 (dMDSCs) 上的调节,损害了它们的功能. 这种功能障碍由SHP-2/STAT6通路介导,可能导致不良妊娠结果.
科学领域:
- 免疫学 免疫学 免疫学
- 生殖生物学 生殖生物学
- 传染性疾病 传染性疾病
背景情况:
- 毒素菌感染对怀孕构成风险,包括流产和胎儿形.
- 脱落性骨髓衍生抑制细胞 (dMDSCs) 对于通过免疫抑制维持正常怀孕至关重要.
- 白细胞免疫球蛋白样受体B4 (LILRB4) 在dMDSCs上高度表达,但其在T. gondii感染中的作用尚不清楚.
研究的目的:
- 调查T. gondii感染对dMDSC中的LILRB4表达的影响.
- 通过改变LILRB4表达来确定T. gondii感染是否诱导dMDSC功能障碍.
主要方法:
- 实验中使用了感染T. gondii的LILRB4缺乏孕妇小鼠.
- 试验室研究涉及感染人类dMDSCs的抗LILRB4抗体治疗.
- 分析的重点是调节dMDSC功能的分子通路.
主要成果:
- 淋巴菌感染减少了STAT3酸化,导致dMDSCs上的LILRB4表达减少.
- 减少LILRB4表达减少了dMDSC中的关键功能 (阿基纳-1,IL-10) 和信号 (p-SHP2,p-STAT6) 分子.
- 确定了SHP-2/STAT6通路是将LILRB4下调与降低的Arg-1和IL-10联系起来的机制.
结论:
- 淋巴菌感染对dMDSCs降低LILRB4的调节,通过SHP-2/STAT6通路引起它们的功能障碍.
- 这种dMDSC功能障碍是由LILRB4减少所驱动的,可能会导致毒素菌的不良妊娠结果.
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