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Ohl K, Fragoulis A, Klemm P, et al. Nrf2 Is a Central Regulator of Metabolic Reprogramming of Myeloid-Derived Suppressor Cells in Steady State and Sepsis. Front Immunol. 2018;9:1552doi: 10.3389/fimmu.2018.01552.
Ohl, K., Fragoulis, A., Klemm, P., Baumeister, J., Klock, W., Verjans, E., Böll, S., Möllmann, J., Lehrke, M., Costa, I., Denecke, B., Schippers, A., Roth, J., Wagner, N., Wruck, C., & Tenbrock, K. (2018). Nrf2 Is a Central Regulator of Metabolic Reprogramming of Myeloid-Derived Suppressor Cells in Steady State and Sepsis. Frontiers in immunology, 91552. https://doi.org/10.3389/fimmu.2018.01552
Ohl, Kim, et al. "Nrf2 Is a Central Regulator of Metabolic Reprogramming of Myeloid-Derived Suppressor Cells in Steady State and Sepsis." Frontiers in immunology vol. 9 (2018): 1552. doi: https://doi.org/10.3389/fimmu.2018.01552
Ohl K, Fragoulis A, Klemm P, Baumeister J, Klock W, Verjans E, Böll S, Möllmann J, Lehrke M, Costa I, Denecke B, Schippers A, Roth J, Wagner N, Wruck C, Tenbrock K. Nrf2 Is a Central Regulator of Metabolic Reprogramming of Myeloid-Derived Suppressor Cells in Steady State and Sepsis. Front Immunol. 2018 Jul 06;9:1552. doi: 10.3389/fimmu.2018.01552. eCollection 2018. PMID: 30034396; PMCID: PMC6043652.
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Front Immunol. 2018 Jul 06;9:1552. doi: 10.3389/fimmu.2018.01552. eCollection 2018.

Nrf2 Is a Central Regulator of Metabolic Reprogramming of Myeloid-Derived Suppressor Cells in Steady State and Sepsis.

Frontiers in immunology

Kim Ohl, Athanassios Fragoulis, Patricia Klemm, Julian Baumeister, Wiebke Klock, Eva Verjans, Svenja Böll, Julia Möllmann, Michael Lehrke, Ivan Costa, Bernd Denecke, Angela Schippers, Johannes Roth, Norbert Wagner, Christoph Wruck, Klaus Tenbrock

Affiliations

  1. Department of Pediatrics, Medical Faculty, RWTH Aachen, Aachen, Germany.
  2. Department of Anatomy and Cell Biology, Medical Faculty, RWTH Aachen, Aachen, Germany.
  3. Department of General Visceral and Transplantation Surgery, Molecular Tumor Biology, Medical Faculty, RWTH Aachen, Aachen, Germany.
  4. Institute of Pharmacology and Toxicology, RWTH Aachen, Aachen, Germany.
  5. Department of Medicine I, Medical Faculty, RWTH Aachen, Aachen, Germany.
  6. Interdisciplinary Centre for Clinical Research (IZKF) Aachen, Medical Faculty, RWTH Aachen, Aachen, Germany.
  7. Institute of Immunology, University of Münster, Münster, Germany.

PMID: 30034396 PMCID: PMC6043652 DOI: 10.3389/fimmu.2018.01552

Abstract

Arising in inflammatory conditions, myeloid-derived suppressor cells (MDSCs) are constantly confronted with intracellular and extracellular reactive oxygen species molecules and oxidative stress. Generating mice with a constitutive activation of Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) we show a pivotal role of the antioxidant stress defense for development of these immune-modulatory cells. These mice are characterized by a massive increase of splenic CD11b

Keywords: LPS; Nrf2; ROS; myeloid-derived suppressor cell; sepsis

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