ArticleHaematologica2026
Immunomodulatory role of megakaryocytes in the hematopoietic niche of myeloproliferative neoplasms.
Article in Haematologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
- Megakaryocytes in myelofibrosis: mechanisms of fibrotic niche remodeling and therapeutic implications.Biomarker research · 2026Review
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6 authors.
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Abstract
Myeloproliferative neoplasms (MPN) are clonal stem cell disorders characterized by dysregulated megakaryopoiesis and expansion of neoplastic hematopoietic stem cells (HSC). Megakaryocytes (MK) not only regulate HSC function, but also shape immune responses within the marrow niche. Using an aging murine model of MPN with MK-restricted JAK2V617F expression, we investigated the immunomodulatory roles of mutant MK. Compared to wild-type MK, aged mutant MK exhibit enhanced antigen uptake and MHC I presentation, secretion of pro-inflammatory cytokines (PF4, TGFβ, IL-1β), and induction of T-cell dysregulation in the marrow niche. In chimeric murine models with co-existing wild-type and JAK2V617F mutant hematopoietic cells, enhanced MK immune activity correlates with mutant cell expansion and MPN development. Single-cell RNA sequencing revealed that aging amplifies JAK2V617F MK-driven immune remodeling. Notably, aged mutant MK showed marked upregulation of long-interspersed element-1 (LINE-1) retrotransposon transcripts alongside elevated innate immune sensors cyclic GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING), implicating retrotransposon activity in niche inflammation. In human MPN marrow, immunohistochemistry detected LINE-1-encoded protein ORF1p in MK from 12 of 13 MPN patients, but not in orthopedic controls (N=5). These findings identify MK as active immune regulators in MPN, with JAK2V617F mutation and aging synergizing to reprogram MK into inflammatory, immune-modulatory niche cells. LINE-1 activation emerges as a potential driver of chronic marrow inflammation, and a targetable mechanism in clonal hematopoiesis and MPN progression.
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