{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:39:38Z","timestamp":1790746778961,"version":"4.1.0"},"reference-count":43,"publisher":"American Society of Hematology","issue":"13","license":[{"start":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T00:00:00Z","timestamp":1782345600000},"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":[[2026,9,24]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Dysregulation of galectins and global protein glycosylation has been reported in various cancers, but their role in myeloproliferative neoplasms (MPNs) remains incompletely understood. We performed single-cell RNA sequencing, which revealed significant enrichment of galectin genes in MPN monocytes. Cell-cell communication analysis predicted monocytes as a pivotal mediator of intercellular interactions and galectin signaling as a robust input\/output pathway in monocytes. We identified elevated expression of galectin-1 (Gal-1, LGALS1) in monocytes from both human MPN samples and mouse models. Mass cytometry profiling of MPN blood samples demonstrated that recombinant Gal-1 (rGal-1) significantly increased levels of multiple inflammatory cytokines in monocytes without affecting other cell types. Incubation of CD14+ monocytes from patients with MPN with rGal-1 markedly increased the transcription and secretion of inflammatory cytokines. Mechanistically, we uncovered cross talk between the toll-like receptor 4 (TLR4) and Gal-1 signaling pathways, as evidenced by protein 3-dimensional modeling and coimmunoprecipitation analyses. Notably, TLR4 inhibition abrogated the Gal-1\u2013mediated proinflammatory effects in monocytes. We further identified NF-\u03baB\u2013dependent signaling as a key downstream effector of Gal-1, as reporter assays demonstrated rGal-1\u2013mediated activation of NF-\u03baB signaling in a TLR4-dependent manner. We corroborated these findings in vivo in a murine model driven by MPLW515L, in which genetic abrogation of Lgals1 ameliorated key MPN disease features, including leukocytosis and splenomegaly. In addition, Gal-1 inhibition suppressed carrageenan-induced thrombosis and inflammation in vivo. In summary, we identify Gal-1 enrichment in MPN monocytes as a driver of monocyte-mediated inflammation through TLR4 and NF-\u03baB activation and uncover a novel therapeutic avenue for MPNs.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2025032631","type":"journal-article","created":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T11:42:06Z","timestamp":1782387726000},"page":"1708-1722","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":2,"title":["Galectin-1 fuels monocyte hyperinflammation and is a novel therapeutic target in myeloproliferative neoplasms"],"prefix":"10.1182","volume":"148","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8598-4472","authenticated-orcid":false,"given":"Fan","family":"He","sequence":"first","affiliation":[{"name":"1Division of Hematology, Department of Medicine, Washington University School of Medicine, St. Louis, MO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9522-7798","authenticated-orcid":false,"given":"Shuyang","family":"Lin","sequence":"additional","affiliation":[{"name":"1Division of Hematology, Department of Medicine, Washington University School of Medicine, St. Louis, MO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3240-8989","authenticated-orcid":false,"given":"Tim","family":"Kong","sequence":"additional","affiliation":[{"name":"1Division of Hematology, Department of Medicine, Washington University School of Medicine, St. Louis, MO"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel A. 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