Takaharu Katagiri,M.D.站在前面和Hiroyasu Nakano,M.D.,Ph.D。,Toho大学医学院教授,站在他的实验室中的其他实验室成员。信贷:托院大学医学院
免疫系统对于防御侵袭病原体是必不可少的,但其异常活化可能导致自身免疫疾病。调节性T细胞在预防过度免疫激活方面发挥至关重要的作用;没有足够的Treg函数的小鼠开发自身免疫性疾病,易受免疫疾病的影响。
“Treg细胞由于其独特的抑制功能而引起了很多关注,但是如何在我们的身体中产生Treg细胞如何完全理解。在一个鼠标模型对于人类溃疡性结肠炎,由于降低Treg细胞数,小鼠缺乏Junb的症状更严重。Junb缺陷的T细胞表现出IL-2生产和IL-2信号传导的损伤。In addition, injection of a high dose of IL-2 into JunB-deficient mice mitigated colitis by expansion of Treg cells," explained the lead author of the paper, Takaharu Katagiri, M.D., who is a graduate student at Toho University working to become a physician-scientist.
"We hope these findings will lead to the development of a novel strategy to treat inflammatory diseases by manipulating the function of JunB," said the senior authors of the study, Soh Yamazaki, Ph.D, Associate Professor, and Hiroyasu Nakano, M.D., Ph.D. Professor of the Toho University School of Medicine. Their finding was published online on July 8th 2019 in the journal粘膜免疫学。
更多信息:Takaharu Katagiri等,Junb通过促进IL-2信号传播在监管T细胞的发展中起着至关重要的作用,粘膜免疫学(2019)。DOI:10.1038 / s41385-019-0182-0
由Toho大学提供
