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SDHA: a key player in T cell-mediated intestinal disease severity

SDHA: a key player in T cell-mediated intestinal disease severity www.nature.com/cmi RESEARCH HIGHLIGHT José M. Izquierdo © The Author(s), under exclusive licence to CSI and USTC 2021 Cellular & Molecular Immunology (2022) 19:139–141; https://doi.org/10.1038/s41423-021-00820-7 In their recent article in Nature Immunology, Fujiwara et al. in IECs from all groups, suggesting that the glycolysis flux was identified reduced mitochondrial respiration and increased succi- refractory, which was confirmed by metabolic isotopic labeling of nate levels in intestinal epithelial cells (IECs) from several distinct glycolysis. To determine the mechanism resulting in the increased models of T cell-mediated colitis. Their observations point to a succinate, the authors experimentally eliminated the contributions specific link between alterations in the mitochondrial complex II of glucose and glutamine anaplerosis and β-oxidation. The component SDHA and the severity of T cell-mediated intestinal researchers hypothesized that the elevated succinate resulted diseases and suggest that SDHA dysfunction could be a diagnostic from the downregulation of SDHA, which catalyzes the oxidation and/or prognostic biomarker in T cell-mediated immunopathology. of succinate to fumarate and generates FADH in the electron Unique metabolic phenotypes are characteristic of several transport chain (ETC). Analysis of SDHA activity in cryosections of human pathologies, which is hardly surprising given the known GVHD target tissues revealed a decrease in http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cellular & Molecular Immunology Springer Journals

SDHA: a key player in T cell-mediated intestinal disease severity

Cellular & Molecular Immunology , Volume 19 (2) – Feb 1, 2022

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References (10)

Publisher
Springer Journals
Copyright
Copyright © The Author(s), under exclusive licence to CSI and USTC 2021
ISSN
1672-7681
eISSN
2042-0226
DOI
10.1038/s41423-021-00820-7
Publisher site
See Article on Publisher Site

Abstract

www.nature.com/cmi RESEARCH HIGHLIGHT José M. Izquierdo © The Author(s), under exclusive licence to CSI and USTC 2021 Cellular & Molecular Immunology (2022) 19:139–141; https://doi.org/10.1038/s41423-021-00820-7 In their recent article in Nature Immunology, Fujiwara et al. in IECs from all groups, suggesting that the glycolysis flux was identified reduced mitochondrial respiration and increased succi- refractory, which was confirmed by metabolic isotopic labeling of nate levels in intestinal epithelial cells (IECs) from several distinct glycolysis. To determine the mechanism resulting in the increased models of T cell-mediated colitis. Their observations point to a succinate, the authors experimentally eliminated the contributions specific link between alterations in the mitochondrial complex II of glucose and glutamine anaplerosis and β-oxidation. The component SDHA and the severity of T cell-mediated intestinal researchers hypothesized that the elevated succinate resulted diseases and suggest that SDHA dysfunction could be a diagnostic from the downregulation of SDHA, which catalyzes the oxidation and/or prognostic biomarker in T cell-mediated immunopathology. of succinate to fumarate and generates FADH in the electron Unique metabolic phenotypes are characteristic of several transport chain (ETC). Analysis of SDHA activity in cryosections of human pathologies, which is hardly surprising given the known GVHD target tissues revealed a decrease in

Journal

Cellular & Molecular ImmunologySpringer Journals

Published: Feb 1, 2022

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