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Howard JE, Smith JNP, Fredman G, et al. IL-18R-mediated HSC quiescence and MLKL-dependent cell death limit hematopoiesis during infection-induced shock. Stem Cell Reports. 2021;16(12):2887-2899doi: 10.1016/j.stemcr.2021.10.011.
Howard, J. E., Smith, J. N. P., Fredman, G., & MacNamara, K. C. (2021). IL-18R-mediated HSC quiescence and MLKL-dependent cell death limit hematopoiesis during infection-induced shock. Stem cell reports, 16(12), 2887-2899. https://doi.org/10.1016/j.stemcr.2021.10.011
Howard, Jennifer E, et al. "IL-18R-mediated HSC quiescence and MLKL-dependent cell death limit hematopoiesis during infection-induced shock." Stem cell reports vol. 16,12 (2021): 2887-2899. doi: https://doi.org/10.1016/j.stemcr.2021.10.011
Howard JE, Smith JNP, Fredman G, MacNamara KC. IL-18R-mediated HSC quiescence and MLKL-dependent cell death limit hematopoiesis during infection-induced shock. Stem Cell Reports. 2021 Dec 14;16(12):2887-2899. doi: 10.1016/j.stemcr.2021.10.011. Epub 2021 Nov 18. PMID: 34798063.
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Stem Cell Reports. 2021 Dec 14;16(12):2887-2899. doi: 10.1016/j.stemcr.2021.10.011. Epub 2021 Nov 18.

IL-18R-mediated HSC quiescence and MLKL-dependent cell death limit hematopoiesis during infection-induced shock.

Stem cell reports

Jennifer E Howard, Julianne N P Smith, Gabrielle Fredman, Katherine C MacNamara

Affiliations

  1. The Department of Immunology and Infectious Disease, Albany Medical College, MC-151 47 New Scotland Avenue, Albany, NY 12208, USA.
  2. The Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA.
  3. The Department of Immunology and Infectious Disease, Albany Medical College, MC-151 47 New Scotland Avenue, Albany, NY 12208, USA. Electronic address: [email protected].

PMID: 34798063 DOI: 10.1016/j.stemcr.2021.10.011

Abstract

Severe infection can dramatically alter blood production, but the mechanisms driving hematopoietic stem and progenitor cell (HSC/HSPC) loss have not been clearly defined. Using Ixodes ovatus Ehrlichia (IOE), a tick-borne pathogen that causes severe shock-like illness and bone marrow (BM) aplasia, type I and II interferons (IFNs) promoted loss of HSPCs via increased cell death and enforced quiescence. IFN-αβ were required for increased interleukin 18 (IL-18) expression during infection, correlating with ST-HSC loss. IL-18 deficiency prevented BM aplasia and increased HSC/HSPCs. IL-18R signaling was intrinsically required for ST-HSC quiescence, but not for HSPC cell death. To elucidate cell death mechanisms, MLKL- or gasdermin D-deficient mice were infected; whereas Mlkl

Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

Keywords: HSC; IL-18; MLKL; cell death; cytokines; hematopoiesis; infection; interferon; shock

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