Institute for Medical Microbiology Hospital Hygiene, Philipps University Marburg, Marburg, Germany.
Flow Cytometry Core Facility BMFZ¸ Philipps University Marburg, Marburg, Germany.
Eur J Immunol. 2019 May;49(5):812-815. doi: 10.1002/eji.201847530. Epub 2018 Sep 30.
We found that deletion of the final 30 amino acids of transcription factor IRF4's (interferon-regulatory factor) C-terminus creates hyperactive IRF4. When introduced into IRF4-deficient CD4 or CD8 T cells, more type 17 differentiation was found compared to WT IRF4. Interestingly, Th9 differentiation and Th2-linked IL-13 production were much less altered.
我们发现,删除转录因子 IRF4(干扰素调节因子)C 端的最后 30 个氨基酸会产生超活性的 IRF4。当将其引入缺乏 IRF4 的 CD4 或 CD8 T 细胞时,与 WT IRF4 相比,发现更多的 17 型分化。有趣的是,Th9 分化和 Th2 相关的 IL-13 产生变化较小。