{"title":"A Compass to Guide Insights into T<sub>H</sub>17 Cellular Metabolism and Autoimmunity.","authors":"Adrianna N Wilson, Sarah A Mosure, Laura A Solt","doi":"10.20900/immunometab20220001","DOIUrl":null,"url":null,"abstract":"<p><p>T cells rapidly convert their cellular metabolic requirements upon activation, switching to a highly glycolytic program to satisfy their increasingly complex energy needs. Fundamental metabolic differences have been established for the development of Foxp3<sup>+</sup> T regulatory (Treg) cells versus T<sub>H</sub>17 cells, alterations of which can drive disease. T<sub>H</sub>17 cell dysregulation is a driver of autoimmunity and chronic inflammation, contributing to pathogenesis in diseases such as multiple sclerosis. A recent paper published in <i>Cell</i> by Wagner, et al. combined scRNA-seq and metabolic mapping data to interrogate potential metabolic modulators of T<sub>H</sub>17 cell pathogenicity. This Compass to T<sub>H</sub>17 cell metabolism highlights the polyamine pathway as a critical regulator of T<sub>H</sub>17/Treg cell function, signifying its potential as a therapeutic target.</p>","PeriodicalId":13361,"journal":{"name":"Immunometabolism","volume":"4 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8654074/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunometabolism","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.20900/immunometab20220001","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
T cells rapidly convert their cellular metabolic requirements upon activation, switching to a highly glycolytic program to satisfy their increasingly complex energy needs. Fundamental metabolic differences have been established for the development of Foxp3+ T regulatory (Treg) cells versus TH17 cells, alterations of which can drive disease. TH17 cell dysregulation is a driver of autoimmunity and chronic inflammation, contributing to pathogenesis in diseases such as multiple sclerosis. A recent paper published in Cell by Wagner, et al. combined scRNA-seq and metabolic mapping data to interrogate potential metabolic modulators of TH17 cell pathogenicity. This Compass to TH17 cell metabolism highlights the polyamine pathway as a critical regulator of TH17/Treg cell function, signifying its potential as a therapeutic target.
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