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 o...

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Detalles Bibliográficos
Autores principales: Mosure, Sarah A., Solt, Laura A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2021
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7894650/
https://www.ncbi.nlm.nih.gov/pubmed/33614166
http://dx.doi.org/10.20900/immunometab20210006
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author Mosure, Sarah A.
Solt, Laura A.
author_facet Mosure, Sarah A.
Solt, Laura A.
author_sort Mosure, Sarah A.
collection PubMed
description 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.
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spelling pubmed-78946502021-02-19 Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity Mosure, Sarah A. Solt, Laura A. Immunometabolism Article 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. 2021-01-22 2021 /pmc/articles/PMC7894650/ /pubmed/33614166 http://dx.doi.org/10.20900/immunometab20210006 Text en http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms and conditions of Creative Commons Attribution 4.0 International License.
spellingShingle Article
Mosure, Sarah A.
Solt, Laura A.
Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity
title Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity
title_full Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity
title_fullStr Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity
title_full_unstemmed Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity
title_short Uncovering New Challenges in Targeting Glycolysis to Treat Th17 Cell-Mediated Autoimmunity
title_sort uncovering new challenges in targeting glycolysis to treat th17 cell-mediated autoimmunity
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7894650/
https://www.ncbi.nlm.nih.gov/pubmed/33614166
http://dx.doi.org/10.20900/immunometab20210006
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