{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T22:28:54Z","timestamp":1791412134777,"version":"4.3.3"},"reference-count":56,"publisher":"American Society of Hematology","issue":"6","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2012,2,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Steady-state hematopoiesis is altered on infection, but the cellular and molecular mechanisms driving these changes are largely unknown. Modulation of hematopoiesis is essential to increase the output of the appropriate type of effector cell required to combat the invading pathogen. In the present study, we demonstrate that the pro-inflammatory cytokine IFN\u03b3 is involved in orchestrating inflammation-induced myelopoiesis. Using both mouse models and in vitro assays, we show that IFN\u03b3 induces the differentiation of monocytes over neutrophils at the level of myeloid progenitors. Infection with lymphocytic choriomeningitis virus induces monopoiesis in wild-type mice, but causes increased neutrophil production in IFN\u03b3\u2212\/\u2212 mice. We demonstrate that IFN\u03b3 enhances the expression of the monopoiesis-inducing transcription factors IRF8 and PU.1 in myeloid progenitor cells, whereas it reduces G-CSF\u2013driven neutrophil differentiation via a SOCS3-dependent inhibition of STAT3 phosphorylation. These results establish a critical role for IFN\u03b3 in directing monocyte versus neutrophil development during immune activation.<\/jats:p>","DOI":"10.1182\/blood-2011-07-367706","type":"journal-article","created":{"date-parts":[[2011,11,24]],"date-time":"2011-11-24T07:36:56Z","timestamp":1322120216000},"page":"1543-1554","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":142,"title":["IFN\u03b3 induces monopoiesis and inhibits neutrophil development during inflammation"],"prefix":"10.1182","volume":"119","author":[{"given":"Alexander M.","family":"de Bruin","sequence":"first","affiliation":[{"name":"Department of Experimental Immunology, Academical Medical Center, Amsterdam, The Netherlands,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sten F.","family":"Libregts","sequence":"additional","affiliation":[{"name":"Department of Experimental Immunology, Academical Medical Center, Amsterdam, The Netherlands,"},{"name":"Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marijke","family":"Valkhof","sequence":"additional","affiliation":[{"name":"Department of Hematology, Erasmus Medical Center, Rotterdam, The Netherlands, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Louis","family":"Boon","sequence":"additional","affiliation":[{"name":"Bioceros BV, Utrecht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivo P.","family":"Touw","sequence":"additional","affiliation":[{"name":"Department of Hematology, Erasmus Medical Center, Rotterdam, The Netherlands, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martijn A.","family":"Nolte","sequence":"additional","affiliation":[{"name":"Department of Experimental Immunology, Academical Medical Center, Amsterdam, The Netherlands,"},{"name":"Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory, Amsterdam, The Netherlands,"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"issue":"11","key":"2019111813075489500_B1","doi-asserted-by":"crossref","first-page":"1771","DOI":"10.1084\/jem.20041419","article-title":"Inflammation and the reciprocal production of granulocytes and lymphocytes in bone marrow.","volume":"201","author":"Ueda","year":"2005","journal-title":"J Exp Med"},{"issue":"12","key":"2019111813075489500_B2","doi-asserted-by":"crossref","first-page":"3725","DOI":"10.1182\/blood.V95.12.3725","article-title":"\u201cEmergency\u201d granulopoiesis in G-CSF-deficient mice in response to Candida albicans infection.","volume":"95","author":"Basu","year":"2000","journal-title":"Blood"},{"issue":"2","key":"2019111813075489500_B3","doi-asserted-by":"crossref","first-page":"306","DOI":"10.1016\/j.immuni.2008.05.019","article-title":"Gr1(+) inflammatory monocytes are required for mucosal resistance to the pathogen Toxoplasma gondii.","volume":"29","author":"Dunay","year":"2008","journal-title":"Immunity"},{"issue":"1","key":"2019111813075489500_B4","doi-asserted-by":"crossref","first-page":"27","DOI":"10.1084\/jem.170.1.27","article-title":"Exacerbation of murine listeriosis by a monoclonal antibody specific for the type 3 complement receptor of myelomonocytic cells. 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