Linking IL-10 signaling with lipid metabolic programs in macrophages:dysregulated ceramide homeostasis drives colitis  

作　　者：Imke Atreya Markus F.Neurath 

机构地区：[1]Department of Medicine 1,University Hospital of Erlangen,Friedrich-Alexander University Erlangen-Nürnberg,Erlangen,Germany [2]Deutsches Zentrum Immuntherapie(DZI),Erlangen,Germany

出　　处：《Signal Transduction and Targeted Therapy》2024年第7期2835-2836,共2页信号转导与靶向治疗（英文）

基　　金：supported by the following grants from the DFG;German Research Foundation:TRR241(project number 375876048);AT 122/2-1(project number 511510453);supported by the Interdisciplinary Center for Clinical Research Erlangen:IZKF D37.

摘　　要：In a recent study published in Nature,York and coworkers identified the immunometabolic regulation of mono-unsaturated fatty acid(MUFA)pools and the subsequent increase in sphingolipid biosynthesis in TLR2-activated macrophages as an important link between impaired IL-10 signaling and the development of intestinal inflammation.1 Thus,targeted interference with the newly identified IL-10/MUFA/sphingolipid axis appears as a promising strategy to restore immunometabolic homeostasis in the intestine of patients with inflammatory bowel diseases(IBD).

关 键 词：HOMEOSTASIS IMPAIRED INTESTINE 

分 类 号：R574[医药卫生—消化系统]