{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T02:20:26Z","timestamp":1787883626158,"version":"build-2784847793"},"reference-count":107,"publisher":"American Society of Hematology","issue":"9","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,8,27]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Heparin-induced thrombocytopenia (HIT) is a common drug-induced immune disorder occurring in a subset of heparin-treated patients. Immune complexes comprising heparin, platelet factor 4 (PF4), and PF4\/heparin-reactive antibodies are central to its pathogenesis. However, the role of epigenetic modification in HIT remains unexplored. Our study identified Jmjd1c, a member of the lysine-specific histone demethylase 3 subfamily, as an essential regulator of PF4\/heparin-specific antibody production. Although Jmjd1c was expressed throughout B-cell development and was dispensable for normal B-cell development, its deficiency disrupted immune tolerance and promoted production of self-reactive antibodies in systemic autoimmune diseases, including PF4\/heparin-specific platelet-activating antibodies, a hallmark of pathogenic HIT antibodies. Jmjd1c-deficient B cells were hyperresponsive, characterized by enhanced B-cell receptor (BCR)\u2013induced proliferation. Transcriptomic analysis (RNA sequencing) revealed upregulation of pathways associated with BCR signaling, NF-\u03baB activation, cell cycle, and systemic lupus erythematosus (SLE). CUT&amp;Tag (cleavage under targets and tagmentation) profiling demonstrated that Jmjd1c deficiency increased H3K36me1 modification at gene start sites in these pathways, indicating that epigenetic dysregulation drives B-cell hyperactivation. Importantly, transcriptional profiling and regulon analysis of B cells from patients with HIT showed enrichment of BCR signaling, cell cycle, NF-\u03baB, and SLE-associated pathways, closely mirroring those in Jmjd1c-deficient B cells. Epigenetic analyses further revealed enhanced promoter chromatin accessibility and elevated H3K36me1 deposition at promoter\u2013transcription start site regions in HIT B cells. All these findings establish a strong molecular overlap between Jmjd1c deficiency and human HIT B cells and reveal a previously unrecognized epigenetic mechanism underlying HIT pathogenesis. To our knowledge, our study provides the first evidence linking epigenetic regulation to HIT, offering new insights into its pathophysiology.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2025029593","type":"journal-article","created":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T14:54:58Z","timestamp":1778165698000},"page":"1175-1190","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":1,"title":["Jmjd1c-mediated epigenetic control of autoimmunity and HIT antibody production"],"prefix":"10.1182","volume":"148","author":[{"given":"Mei","family":"Yu","sequence":"first","affiliation":[{"name":"1Versiti Blood Research Institute, Milwaukee, WI"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lu","family":"Zhou","sequence":"additional","affiliation":[{"name":"1Versiti Blood Research Institute, Milwaukee, WI"},{"name":"2Department of Microbiology and Immunology, Medical College of Wisconsin, 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