{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T12:38:22Z","timestamp":1793363902681,"version":"4.5.0"},"reference-count":78,"publisher":"American Society of Hematology","issue":"6","license":[{"start":{"date-parts":[[2025,5,15]],"date-time":"2025-05-15T00:00:00Z","timestamp":1747267200000},"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":[[2025,8,7]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Myeloproliferative neoplasms (MPNs) are hematopoietic stem cell\u2013driven malignancies marked by excessive myelopoiesis and high risk of myelofibrosis, which remains therapeutically challenging. Senescent neutrophils home daily to the bone marrow (BM) to be cleared by macrophages. This avoids their accumulation, which can increase the risk of chronic inflammation or oncogenesis. Neutrophils carrying the most common oncogenic MPN driver (JAK2V617F) are protected from apoptosis, which may prolong their life span and enhance their proinflammatory activity. In contrast, abnormal interactions of neutrophils with megakaryocytes (\u201cemperipolesis\u201d) have been associated with BM fibrosis in disparate hematologic disorders, including MPN and gray platelet syndrome; however, the underlying pathophysiology remains unclear. We investigated neutrophil homeostasis and cellular interactions in MPN. We found that senescent neutrophils evade homeostatic clearance and accumulate in JAK2V617F MPN, but not in MPN caused by the second most prevalent mutations affecting calreticulin gene. This is explained by granulocyte-macrophage colony-stimulating factor-JAK2-STAT5\u2013dependent upregulation of the \u201cdon\u2019t eat me\u201d signal CD24 in neutrophils. Mechanistically, JAK2V617F CD24hi neutrophils evade efferocytosis, invade megakaryocytes, and increase active transforming growth factor \u03b2 (TGF-\u03b2). Collectively, JAK2V617F neutrophil-megakaryocyte interactions promote platelet production in a humanized bioreactor and myelofibrosis in mouse models. Notably, chronic antibody blockade or genetic loss of CD24 restores clearance of senescent neutrophils and reduces emperipolesis and active TGF-\u03b2. Consequently, CD24 blockade improves thrombocytosis and prevents myelofibrosis in MPN mice. Taken together, these findings reveal defective neutrophil clearance as a cause of pathogenic microenvironmental interactions of inflammatory neutrophils with megakaryocytes, associated with myelofibrosis in MPN. Our study postulates CD24 as a candidate innate immune checkpoint in MPN.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2024027455","type":"journal-article","created":{"date-parts":[[2025,5,15]],"date-time":"2025-05-15T16:16:18Z","timestamp":1747325778000},"page":"717-731","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":27,"title":["Defective neutrophil clearance in\n                    <i>JAK2<\/i>\n                    <i>V617F<\/i>\n                    myeloproliferative neoplasms drives myelofibrosis via immune checkpoint CD24"],"prefix":"10.1182","volume":"146","author":[{"given":"Eman","family":"Khatib-Massalha","sequence":"first","affiliation":[{"name":"1Cambridge Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom"},{"name":"2Department of Haematology, University of Cambridge, Cambridge, United Kingdom"},{"name":"3NHS Blood and Transplant, Cambridge, United 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Haematology, University of Cambridge, Cambridge, United Kingdom"},{"name":"3NHS Blood and Transplant, Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-3119-6664","authenticated-orcid":false,"given":"Jos\u00e9","family":"Quesada-Salas","sequence":"additional","affiliation":[{"name":"5Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Roc\u00edo\/CSIC\/Universidad de Sevilla, Seville, Spain"},{"name":"6Department of Medical Physiology and Biophysics, University of Seville, Seville, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eva","family":"Carrillo F\u00e9lez","sequence":"additional","affiliation":[{"name":"1Cambridge Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom"},{"name":"2Department of Haematology, University of Cambridge, Cambridge, United Kingdom"},{"name":"3NHS Blood and Transplant, Cambridge, United 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