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We report a novel role for the miR-145 target, Toll\/interleukin-1 receptor domain containing adaptor protein (TIRAP), in driving bone marrow failure. We show that TIRAP is overexpressed in various types of myelodysplastic syndromes (MDS) and suppresses all three major hematopoietic lineages. TIRAP expression promotes up-regulation of Ifn\u03b3, leading to myelosuppression through Ifn\u03b3-Ifn\u03b3r\u2013mediated release of the alarmin, Hmgb1, which disrupts the bone marrow endothelial niche. Deletion of Ifn\u03b3 blocks Hmgb1 release and is sufficient to reverse the endothelial defect and restore myelopoiesis. Contrary to current dogma, TIRAP-activated Ifn\u03b3-driven bone marrow suppression is independent of T cell function or pyroptosis. In the absence of Ifn\u03b3, TIRAP drives myeloproliferation, implicating Ifn\u03b3 in suppressing the transformation of MDS to acute leukemia. These findings reveal novel, noncanonical roles of TIRAP, Hmgb1, and Ifn\u03b3 in the bone marrow microenvironment and provide insight into the pathophysiology of preleukemic syndromes.<\/jats:p>","DOI":"10.1084\/jem.20200731","type":"journal-article","created":{"date-parts":[[2021,12,17]],"date-time":"2021-12-17T02:22:01Z","timestamp":1639707721000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":22,"title":["TIRAP drives myelosuppression through an Ifn\u03b3\u2013Hmgb1 axis that disrupts the endothelial niche in mice"],"prefix":"10.1084","volume":"219","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9757-9896","authenticated-orcid":true,"given":"Aparna","family":"Gopal","sequence":"first","affiliation":[{"name":"Michael Smith Genome Sciences Centre, BC Cancer Research Institute, Vancouver, British Columbia, Canada 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