Glucocorticoid receptor promotes the function of myeloid-derived suppressor cells by suppressing HIF1α-dependent glycolysis
作者机构：Department of ImmunologySchool of Basic Medical SciencesFudan UniversityShanghai 200032China Key Laboratory of Cell Proliferation and Regulation Biology of Ministry of EducationInstitute of Cell BiologyCollege of Life SciencesBeijing Normal UniversityBeijing 100875China State Key laboratory of Pathogen and BiosecurityBeijing Institute of Microbiology and EpidemiologyBeijing 100071China State Key Laboratory of Membrane BiologyInstitute of ZoologyChinese Academy of SciencesBeijing 100101China Center for Childhood Cancer and Blood DiseasesHematology/Oncology and BMTThe Research Institute at Nationwide Children's HospitalOhio State UniversityColumbusOhio 43205USA
出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)
年 卷 期：2018年第15卷第6期
页 面：618-629页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
基 金：This research is supported by grants from the National Natural Science Foundation for General Programs of China(31671524,31171407 and 81273201,GL) the Key Basic Research Project of the Science and Technology Commission of Shanghai Municipality(12JC1400900,GL) the Innovation Program of Shanghai Municipal Education Commission(14ZZ009,GL) the Excellent Youth Foundation of Chinese Academy of Sciences(KSCX2-EW-Q-7,GL) R21AI117547,1R01AI114581,V2014-001 from the V-foundation,and 128436-RSG-15-180-01-LIB from the American Cancer Society(RW)
主 题：glucocorticoid-receptor glycolysis innate immunity liver injuries metabolism myeloid-derived suppressive cells tolerance
摘 要：Immunomodulatory signaling imposes tight regulations on metabolic programs within immune cells and consequentially determines immune response *** the glucocorticoid receptor(GR)has been recently implicated in regulating the function of myeloid-derived suppressor cells(MDSCs),whether the dysregulation of GR in MDSCs is involved in immune-mediated hepatic diseases and how GR regulates the function of MDSCs in such a context remains ***,we revealed the dysregulation of GR expression in MDSCs during innate immunological hepatic injury(IMH)and found that GR regulates the function of MDSCs through modulating HIF1α-dependent *** modulation of GR by its agonist(dexamethasone,Dex)protects IMH mice against inflammatory ***,GR signaling suppresses HIF1αand HIF1α-dependent glycolysis in MDSCs and thus promotes the immune suppressive activity of *** studies reveal a role of GR-HIF1αin regulating the metabolism and function of MDSCs and further implicate MDSC GR signaling as a potential therapeutic target in hepatic diseases that are driven by innate immune cell-mediated systemic inflammation.
维普期刊数据库