靶向糖酵解治疗Th17细胞介导的自身免疫的新挑战

Immunometabolism Pub Date : 2021-01-01 Epub Date: 2021-01-22 DOI:10.20900/immunometab20210006
Sarah A Mosure, Laura A Solt
{"title":"靶向糖酵解治疗Th17细胞介导的自身免疫的新挑战","authors":"Sarah A Mosure,&nbsp;Laura A Solt","doi":"10.20900/immunometab20210006","DOIUrl":null,"url":null,"abstract":"<p><p>Targeting glycolysis in T helper 17 (Th17) cells presents an attractive opportunity to treat Th17 cell-mediated autoimmune diseases such as multiple sclerosis (MS). Pyruvate kinase isoform 2 (PKM2) is a glycolytic enzyme expressed in T cells infiltrating the central nervous system in a mouse model of MS, suggesting PKM2 modulation could provide a new avenue for MS therapeutics. In a recent article in <i>Science Signaling</i>, Seki et al. show that pharmacological modulation of PKM2 alters but does not ameliorate disease in a mouse model of MS. These results warrant further consideration of PKM2 modulators to treat Th17 cell-mediated autoimmunity.</p>","PeriodicalId":13361,"journal":{"name":"Immunometabolism","volume":"3 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7894650/pdf/","citationCount":"2","resultStr":"{\"title\":\"Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity.\",\"authors\":\"Sarah A Mosure,&nbsp;Laura A Solt\",\"doi\":\"10.20900/immunometab20210006\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Targeting glycolysis in T helper 17 (Th17) cells presents an attractive opportunity to treat Th17 cell-mediated autoimmune diseases such as multiple sclerosis (MS). Pyruvate kinase isoform 2 (PKM2) is a glycolytic enzyme expressed in T cells infiltrating the central nervous system in a mouse model of MS, suggesting PKM2 modulation could provide a new avenue for MS therapeutics. In a recent article in <i>Science Signaling</i>, Seki et al. show that pharmacological modulation of PKM2 alters but does not ameliorate disease in a mouse model of MS. These results warrant further consideration of PKM2 modulators to treat Th17 cell-mediated autoimmunity.</p>\",\"PeriodicalId\":13361,\"journal\":{\"name\":\"Immunometabolism\",\"volume\":\"3 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2021-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7894650/pdf/\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Immunometabolism\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.20900/immunometab20210006\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/1/22 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunometabolism","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.20900/immunometab20210006","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/1/22 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2

摘要

靶向T辅助17 (Th17)细胞的糖酵解为治疗Th17细胞介导的自身免疫性疾病(如多发性硬化症(MS))提供了一个有吸引力的机会。丙酮酸激酶异构体2 (Pyruvate kinase isoform 2, PKM2)是一种在MS小鼠模型中浸润中枢神经系统的T细胞中表达的糖酵解酶,这表明PKM2的调节可能为MS的治疗提供新的途径。在Science Signaling最近的一篇文章中,Seki等人表明,在ms小鼠模型中,PKM2的药理学调节改变了但并没有改善疾病。这些结果值得进一步考虑PKM2调节剂来治疗Th17细胞介导的自身免疫。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity.

Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity.

Targeting glycolysis in T helper 17 (Th17) cells presents an attractive opportunity to treat Th17 cell-mediated autoimmune diseases such as multiple sclerosis (MS). Pyruvate kinase isoform 2 (PKM2) is a glycolytic enzyme expressed in T cells infiltrating the central nervous system in a mouse model of MS, suggesting PKM2 modulation could provide a new avenue for MS therapeutics. In a recent article in Science Signaling, Seki et al. show that pharmacological modulation of PKM2 alters but does not ameliorate disease in a mouse model of MS. These results warrant further consideration of PKM2 modulators to treat Th17 cell-mediated autoimmunity.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信