{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T19:57:14Z","timestamp":1793735834155,"version":"4.6.1"},"reference-count":56,"publisher":"American Society of Hematology","issue":"11","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,9,10]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Polycythemia vera (PV) is a clonal hematopoietic stem cell disorder resulting in overproduction of erythrocytes. Although interferon alfa (IFN-\u03b1) has shown therapeutic efficacy in PV and other myeloproliferative neoplasms (MPN), its precise mechanism of action remains poorly understood. In this study, we identify natural killer (NK) cells as primary immune effectors responsive to IFN-\u03b1 treatment in PV essential for disease control in vivo. Using a transgenic mouse model of PV, we demonstrate that IFN-\u03b1 induces the expansion of CD27+ NK cells in the bone marrow. In patients with PV or essential thrombocythemia undergoing IFN-\u03b1 therapy, the frequency of CD56bright NK cells is increased and correlates with the molecular response. Depletion of NK cells abrogated the therapeutic effects of IFN-\u03b1. In vitro experiments demonstrate that NK cells preferentially killed Jak2VF mutant hematopoietic stem and progenitor cells in a tumor necrosis factor-\u03b1\u2013dependent manner and independent of IFN-\u03b3 or NKG2D. Notably, PV mice depleted of NK cells or lacking type-I interferon receptor on NK cells showed accelerated disease progression in the absence of exogenous IFN-\u03b1. This suggests that direct sensing of basal levels of type-I interferons by NK cells is essential for attenuating disease progression, emphasizing a critical role for NK cells in immune surveillance of MPN. These findings offer new insights into type-I interferon-mediated immune modulation in MPN and highlight the potential of NK cell activation to improve therapeutic outcomes.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2026033951","type":"journal-article","created":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T11:10:41Z","timestamp":1780485041000},"page":"1454-1465","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":2,"title":["Type-I interferon\u2013activated NK cells control polycythemia vera in vivo"],"prefix":"10.1182","volume":"148","author":[{"given":"Johanna","family":"Lossa","sequence":"first","affiliation":[{"name":"1Institute of Immunology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany"},{"name":"2Research Center for Immunotherapy, University Medical Center of the Johannes Gutenberg University, Mainz, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6351-4119","authenticated-orcid":false,"given":"Tina M.","family":"Schn\u00f6der","sequence":"additional","affiliation":[{"name":"3Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, Hannover, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zora","family":"Ronge","sequence":"additional","affiliation":[{"name":"1Institute of Immunology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany"},{"name":"2Research Center for Immunotherapy, University Medical Center of the Johannes Gutenberg University, Mainz, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nelly","family":"Haasch","sequence":"additional","affiliation":[{"name":"1Institute of Immunology, University Medical Center of the Johannes Gutenberg University, Mainz, Germany"},{"name":"2Research Center for Immunotherapy, 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