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Romance of the three kingdoms: RORgammat allies with HIF1alpha against FoxP3 in regulating T cell metabolism and differentiation

查看全文 作　　者：Andy [1]Tsun;Zuojia [1]Chen;Bin [1]Li 高影响力作者 机构地区：[1]Key Laboratory of Molecular Virology&Immunology,Unit of Molecular Immunology,Institut Pasteur of Shanghai,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai 200025,China高影响力机构 出　　处：《Protein & Cell》索引2011年第2卷第10期,共4页高影响力期刊 基　　金：funds from NSFC(Grant Nos.30972702 and 31050110129);SMCST09JC1416100,Shanghai Pasteur Foundation,Shanghai“Rising Star”program 10QA1407900,China-Germany PPP program,Novo Nordisk-Chinese Academy of Sciences(NN-CAS)Foundation,CAS“100-talents”program,CAS“International Young Scientist Fellowship”,and the Sanofi-Aventis-Shanghai Institutes for Biological Sciences(SA-SIBS)scholarship program. 摘　　要：Regulatory T(Treg)cells play an essential role in immune homeostasis by controlling the function of various immune effector cells,including RAR-related orphan receptor gammat+(RORγt+)T helper 17(Th17)cells.Foekhead box P3(FoxP3)is the master regulator of Treg cell function,while RORγt is the key transcription factor for the induction of the interleukin(IL)-17 family of cytokines during Th17 cell differentiation.FoxP3 can directly interact with and negatively regulate the function of RORγt,to determine the balance between induced Treg(iTreg)and Th17 cell polarization.Two recent independent studies from the Pan and Chi Labs have shown how hypoxia-inducible factor 1 alpha(HIF1α)is able to tip the balance of T cell differentiation toward the Th17 lineage by responding to the local changes in metabolic shift or an increase in proinflammatory mediators in the microenvironment.By allying with HIF1α,RORγt wins the fight against FoxP3 and Treg cell commitment. 关 键 词：FOXP3 RORΓT TH17
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