{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T05:49:53Z","timestamp":1793944193323,"version":"4.8.0"},"reference-count":53,"publisher":"American Society of Hematology","issue":"13","license":[{"start":{"date-parts":[[2025,7,11]],"date-time":"2025-07-11T00:00:00Z","timestamp":1752192000000},"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":[[2025,9,25]]},"abstract":"<jats:sec>\n                  <jats:title>Abstract<\/jats:title>\n                  <jats:p>The megakaryocytic (MK)-specific immunoreceptor G6b-B plays an essential role in MK development. Because germ line loss-of-function mutations of G6b-B in humans and its deletion in mouse models lead to thrombocytopenia and a myelofibrosis-like clinical phenotype (MF-MPIG6B), we explored the role of G6b-B in patients with myelofibrosis (MF) due to a myeloproliferative neoplasm (MPN) with thrombocytopenia (MPN-MF-T). We demonstrated that MKs generated from mononuclear cells (MNCs) from a patient with MF-MPIG6B as well as patients with MPN-MF-T failed to express GATA binding protein 1 and G6B and possessed a protein pattern expression characteristic of MKs primed for inflammation rather than platelet production. MNCs from patients with MPN-MF-T also generated fewer MK-biased hematopoietic stem cells and greater numbers of small cytoplasmic immature MKs (CD41+CD42\u2212G6B\u2212) as compared with MNCs from patients with nonthrombocytopenic MPN-MF (MPN-MF-NT). Plasma levels of transforming growth factor \u03b21 (TGF\u03b21) and chitinase-3-like protein (CHI3L1) also known as YKL-40, which were shown to arrest normal MK maturation, were elevated in the patients with MF-MPIG6B. Although TGF\u03b21 plasma levels were similarly elevated in patients with MPN-MF-T and MPN-MF-NT, tumor necrosis factor \u03b1 (TNF\u03b1) and YKL-40 levels were upregulated to a greater extent in patients with MPN-MF-T than those with MPN-MF-NT. Moreover, we identified a reciprocal positive regulatory loop involving TGF\u03b21 and YKL-40 in MF MKs. These findings indicate that impaired MK maturation, and reduced G6B expression lead to the predominance of proinflammatory MKs, which produce factors that further arrest MK development in patients with MF-MPIG6B and MPN-MF-T patients. This trial was registered at www.clinicaltrials.gov as #NCT03895112.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1182\/blood.2024027363","type":"journal-article","created":{"date-parts":[[2025,7,11]],"date-time":"2025-07-11T12:16:27Z","timestamp":1752236187000},"page":"1612-1624","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":10,"title":["Thrombocytopenia in myelofibrosis is characterized by inflammatory megakaryocytes with reduced G6B expression"],"prefix":"10.1182","volume":"146","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-8273-1520","authenticated-orcid":false,"given":"Lilian","family":"Varricchio","sequence":"first","affiliation":[{"name":"1Division of Hematology and Oncology, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gohar","family":"Mosoyan","sequence":"additional","affiliation":[{"name":"2Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sebastian","family":"Elghaity-Beckley","sequence":"additional","affiliation":[{"name":"1Division of Hematology and Oncology, The Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0372-9310","authenticated-orcid":false,"given":"Md. 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