{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T22:50:58Z","timestamp":1740178258303,"version":"3.37.3"},"reference-count":56,"publisher":"American Society of Hematology","issue":"21","license":[{"start":{"date-parts":[[2024,8,29]],"date-time":"2024-08-29T00:00:00Z","timestamp":1724889600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,11,12]]},"abstract":"<jats:sec>\n                  <jats:title>Abstract<\/jats:title>\n                  <jats:p>Hematopoietic stem cells (HSCs) readily recover from acute stress, but persistent stress can reduce their viability and long-term potential. Here, we show that the nuclear factor of activated T cells 5 (NFAT5), a transcription modulator of inflammatory responses, protects the HSC pool under stress. NFAT5 restrains HSC differentiation to multipotent progenitors after bone marrow transplantation and bone marrow ablation with ionizing radiation or chemotherapy. Correspondingly, NFAT5-deficient HSCs fail to support long-term reconstitution of hematopoietic progenitors and mature blood cells after serial transplant. Evidence from competitive transplant assays shows that these defects are HSC intrinsic. NFAT5-deficient HSCs exhibit enhanced expression of type 1 interferon (IFN-1) response genes after transplant, and suppressing IFN-1 receptor prevents their exacerbated differentiation and cell death after reconstitution and improves long-term regeneration potential. Blockade of IFN-1 receptor also prevented the overdifferentiation of NFAT5-deficient HSCs after bone marrow ablation. These findings show that long-term IFN-1 responses to different hematopoietic stressors drive HSCs toward more differentiated progenitors, and that NFAT5 has an HSC-intrinsic role, limiting IFN-1 responses to preserve reconstitution potential. Our identification of cell-intrinsic mechanisms that strengthen the resistance of HSCs to stress could help to devise approaches to protect long-term stemness during the treatment of hematopoietic malignancies.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1182\/bloodadvances.2023011306","type":"journal-article","created":{"date-parts":[[2024,8,29]],"date-time":"2024-08-29T19:55:04Z","timestamp":1724961304000},"page":"5510-5526","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":0,"title":["NFAT5 counters long-term IFN-1 responses in hematopoietic stem cells to preserve reconstitution potential"],"prefix":"10.1182","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1588-5035","authenticated-orcid":false,"given":"Laia","family":"Traveset","sequence":"first","affiliation":[{"name":"1Department of Medicine and Life Sciences, Immunology Unit, Universitat Pompeu Fabra, Barcelona, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3711-0057","authenticated-orcid":false,"given":"V\u00edctor","family":"Cerd\u00e1n Porqueras","sequence":"additional","affiliation":[{"name":"1Department of Medicine and Life Sciences, Immunology Unit, Universitat Pompeu Fabra, Barcelona, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3723-8624","authenticated-orcid":false,"given":"Hector","family":"Huerga Encabo","sequence":"additional","affiliation":[{"name":"1Department of Medicine and Life Sciences, Immunology Unit, Universitat Pompeu Fabra, Barcelona, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-8384-7264","authenticated-orcid":false,"given":"Silvia","family":"Avalle","sequence":"additional","affiliation":[{"name":"1Department of Medicine and Life Sciences, Immunology Unit, Universitat Pompeu Fabra, Barcelona, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0361-2873","authenticated-orcid":false,"given":"Anna","family":"Esteve-Codina","sequence":"additional","affiliation":[{"name":"2Bioinformatics unit, Centro Nacional de An\u00e1lisis Gen\u00f3mico, Centre for Genomic Regulation, Barcelona Institute for Science and Technology, Barcelona, Spain"},{"name":"3Department of Medicine and Life Sciences, Universitat Pompeu Fabra, Barcelona, Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2017-9100","authenticated-orcid":false,"given":"Oscar","family":"Fornas","sequence":"additional","affiliation":[{"name":"4Department of Medicine and Life Sciences, Flow Cytometry Unit, Universitat Pompeu Fabra, Centre for Genomic Regulation, Barcelona Institute for Science and Technology, Barcelona, 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