{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:40:05Z","timestamp":1790746805866,"version":"4.1.0"},"reference-count":46,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T00:00:00Z","timestamp":1764115200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T00:00:00Z","timestamp":1764115200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Nat Commun"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The development of Philadelphia chromosome-negative classical myeloproliferative neoplasms (MPN) involves an inflammatory process that facilitates outgrowth of the malignant clone and correlates with clinical outcome measures. This raises the question to which extent inflammatory circuits in MPN depend on activation of innate immune sensors. Here, we investigate whether NLRP3, which precipitates inflammasome assembly upon detection of cellular stress, drives murine JAK2V617F mutant MPN. Deletion of\n                    <jats:italic>Nlrp3<\/jats:italic>\n                    within the hematopoietic compartment completely prevents increased IL-1\u03b2 and IL-18 release in MPN. NLRP3 in JAK2V617F hematopoietic cells, but not in JAK2 wild type radioresistant cells, promotes excessive platelet production via stimulation of the direct thrombopoiesis differentiation pathway, as well as granulocytosis. It also promotes expansion of the hematopoietic stem and progenitor cell compartment despite inducing pyroptosis at the same time. Importantly, NLRP3 inflammasome activation enhances bone marrow fibrosis and splenomegaly. Pharmacological blockade of NLRP3 in fully established disease leads to regression of thrombocytosis, splenomegaly and bone marrow fibrosis. These findings suggest that NLRP3 is critical for MPN development and its inhibition represents a new therapeutic intervention for MPN patients.\n                  <\/jats:p>","DOI":"10.1038\/s41467-025-65673-4","type":"journal-article","created":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T12:35:49Z","timestamp":1764160549000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["NLRP3-induced systemic inflammation controls the development of JAK2V617F mutant myeloproliferative neoplasms"],"prefix":"10.1038","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8773-8221","authenticated-orcid":false,"given":"Ruth-Miriam","family":"Koerber","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Calvin","family":"Krollmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin","family":"Cieslak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elisabeth","family":"Tregel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-0060-665X","authenticated-orcid":false,"given":"Maria L.","family":"Saenz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9677-3723","authenticated-orcid":false,"given":"Tim H.","family":"Br\u00fcmmendorf","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1011-8171","authenticated-orcid":false,"given":"Steffen","family":"Koschmieder","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Griesshammer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ines","family":"G\u00fctgemann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Conny K.","family":"Baldauf","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Fischer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Brossart","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carl Christian","family":"Kolbe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1488-5666","authenticated-orcid":false,"given":"Eicke","family":"Latz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4761-075X","authenticated-orcid":false,"given":"Dominik","family":"Wolf","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9489-7282","authenticated-orcid":false,"given":"Lino L.","family":"Teichmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,11,26]]},"reference":[{"key":"65673_CR1","doi-asserted-by":"publisher","first-page":"101","DOI":"10.1146\/annurev-pathol-012615-044454","volume":"11","author":"J Nangalia","year":"2016","unstructured":"Nangalia, J., Grinfeld, J. & Green, A. R. Pathogenesis of myeloproliferative disorders. Annu. Rev. Pathol. Mech. Dis. 11, 101\u2013126 (2016).","journal-title":"Annu. Rev. Pathol. Mech. Dis."},{"key":"65673_CR2","doi-asserted-by":"publisher","first-page":"469","DOI":"10.1182\/blood.2019001113","volume":"134","author":"S Cordua","year":"2019","unstructured":"Cordua, S. et al. Prevalence and phenotypes of JAK2 V617F and calreticulin mutations in a Danish general population. Blood 134, 469\u2013479 (2019).","journal-title":"Blood"},{"key":"65673_CR3","doi-asserted-by":"publisher","first-page":"667","DOI":"10.1182\/blood-2016-10-695940","volume":"129","author":"W Vainchenker","year":"2017","unstructured":"Vainchenker, W. & Kralovics, R. Genetic basis and molecular pathophysiology of classical myeloproliferative neoplasms. Blood 129, 667\u2013679 (2017).","journal-title":"Blood"},{"key":"65673_CR4","doi-asserted-by":"publisher","first-page":"287","DOI":"10.3389\/fonc.2018.00287","volume":"8","author":"E Bousoik","year":"2018","unstructured":"Bousoik, E. & Montazeri Aliabadi, H. \u201cDo we know Jack\u201d about JAK? A closer look at JAK\/STAT signaling pathway. Front. Oncol. 8, 287 (2018).","journal-title":"Front. Oncol."},{"key":"65673_CR5","doi-asserted-by":"publisher","first-page":"6392","DOI":"10.1182\/blood-2011-04-348144","volume":"118","author":"AG Fleischman","year":"2011","unstructured":"Fleischman, A. G. et al. TNF\u03b1 facilitates clonal expansion of JAK2V617F positive cells in myeloproliferative neoplasms. Blood 118, 6392\u20136398 (2011).","journal-title":"Blood"},{"key":"65673_CR6","doi-asserted-by":"publisher","first-page":"1356","DOI":"10.1200\/JCO.2010.32.9490","volume":"29","author":"A Tefferi","year":"2011","unstructured":"Tefferi, A. et al. Circulating interleukin (IL)-8, IL-2R, IL-12, and IL-15 levels are independently prognostic in primary myelofibrosis: a comprehensive cytokine profiling study. JCO 29, 1356\u20131363 (2011).","journal-title":"JCO"},{"key":"65673_CR7","doi-asserted-by":"publisher","first-page":"315","DOI":"10.3324\/haematol.2010.031070","volume":"96","author":"T Barbui","year":"2011","unstructured":"Barbui, T. et al. Inflammation and thrombosis in essential thrombocythemia and polycythemia vera: different role of C-reactive protein and pentraxin 3. Haematologica 96, 315\u2013318 (2011).","journal-title":"Haematologica"},{"key":"65673_CR8","doi-asserted-by":"publisher","first-page":"30","DOI":"10.1038\/s41556-022-01053-0","volume":"25","author":"CA Mitchell","year":"2023","unstructured":"Mitchell, C. A. et al. Stromal niche inflammation mediated by IL-1 signalling is a targetable driver of haematopoietic ageing. Nat. Cell Biol. 25, 30\u201341 (2023).","journal-title":"Nat. Cell Biol."},{"key":"65673_CR9","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-022-32928-3","volume":"13","author":"MF-U Rahman","year":"2022","unstructured":"Rahman, M. F.-U. et al. Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm. Nat. Commun. 13, 5347 (2022).","journal-title":"Nat. Commun."},{"key":"65673_CR10","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-022-32927-4","volume":"13","author":"S Rai","year":"2022","unstructured":"Rai, S. et al. Inhibition of interleukin-1\u03b2 reduces myelofibrosis and osteosclerosis in mice with JAK2-V617F driven myeloproliferative neoplasm. Nat. Commun. 13, 5346 (2022).","journal-title":"Nat. Commun."},{"key":"65673_CR11","doi-asserted-by":"publisher","first-page":"660","DOI":"10.1038\/nature15514","volume":"526","author":"J Shi","year":"2015","unstructured":"Shi, J. et al. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death. Nature 526, 660\u2013665 (2015).","journal-title":"Nature"},{"key":"65673_CR12","doi-asserted-by":"publisher","first-page":"50","DOI":"10.1016\/j.immuni.2019.05.005","volume":"51","author":"SD Tyrkalska","year":"2019","unstructured":"Tyrkalska, S. D. et al. Inflammasome regulates hematopoiesis through cleavage of the master erythroid transcription factor GATA1. Immunity 51, 50\u201363.e5 (2019).","journal-title":"Immunity"},{"key":"65673_CR13","doi-asserted-by":"publisher","first-page":"1035","DOI":"10.1016\/j.it.2019.09.005","volume":"40","author":"Y Xue","year":"2019","unstructured":"Xue, Y., Enosi Tuipulotu, D., Tan, W. H., Kay, C. & Man, S. M. Emerging activators and regulators of inflammasomes and pyroptosis. Trends Immunol. 40, 1035\u20131052 (2019).","journal-title":"Trends Immunol."},{"key":"65673_CR14","doi-asserted-by":"publisher","first-page":"1201","DOI":"10.1038\/s41423-022-00922-w","volume":"19","author":"A Akbal","year":"2022","unstructured":"Akbal, A. et al. How location and cellular signaling combine to activate the NLRP3 inflammasome. Cell Mol. Immunol. 19, 1201\u20131214 (2022).","journal-title":"Cell Mol. Immunol."},{"key":"65673_CR15","doi-asserted-by":"publisher","first-page":"2960","DOI":"10.1182\/blood-2016-07-730556","volume":"128","author":"AA Basiorka","year":"2016","unstructured":"Basiorka, A. A. et al. The NLRP3 inflammasome functions as a driver of the myelodysplastic syndrome phenotype. Blood 128, 2960\u20132975 (2016).","journal-title":"Blood"},{"key":"65673_CR16","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-020-15497-1","volume":"11","author":"S Hamarsheh","year":"2020","unstructured":"Hamarsheh, S. et al. Oncogenic KrasG12D causes myeloproliferation via NLRP3 inflammasome activation. Nat. Commun. 11, 1659 (2020).","journal-title":"Nat. Commun."},{"key":"65673_CR17","doi-asserted-by":"publisher","first-page":"606","DOI":"10.1016\/j.humimm.2020.09.001","volume":"81","author":"Y Zhou","year":"2020","unstructured":"Zhou, Y. et al. Genetic polymorphisms and expression of NLRP3 inflammasome-related genes are associated with Philadelphia chromosome-negative myeloproliferative neoplasms. Hum. Immunol. 81, 606\u2013613 (2020).","journal-title":"Hum. Immunol."},{"key":"65673_CR18","doi-asserted-by":"publisher","first-page":"296","DOI":"10.1038\/s41586-021-03341-5","volume":"592","author":"TP Fidler","year":"2021","unstructured":"Fidler, T. P. et al. The AIM2 inflammasome exacerbates atherosclerosis in clonal haematopoiesis. Nature 592, 296\u2013301 (2021).","journal-title":"Nature"},{"key":"65673_CR19","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2023.1161832","volume":"14","author":"G De Luca","year":"2023","unstructured":"De Luca, G. et al. High cell-free DNA is associated with disease progression, inflammasome activation and elevated levels of inflammasome-related cytokine IL-18 in patients with myelofibrosis. Front. Immunol. 14, 1161832 (2023).","journal-title":"Front. Immunol."},{"key":"65673_CR20","doi-asserted-by":"publisher","first-page":"1292","DOI":"10.1016\/j.molcel.2019.01.009","volume":"73","author":"A Rodriguez-Meira","year":"2019","unstructured":"Rodriguez-Meira, A. et al. Unravelling intratumoral heterogeneity through high-sensitivity single-cell mutational analysis and parallel RNA sequencing. Mol. Cell 73, 1292\u20131305.e8 (2019).","journal-title":"Mol. Cell"},{"key":"65673_CR21","doi-asserted-by":"publisher","first-page":"1117","DOI":"10.1056\/NEJMoa1002028","volume":"363","author":"S Verstovsek","year":"2010","unstructured":"Verstovsek, S. et al. Safety and efficacy of INCB018424, a JAK1 and JAK2 inhibitor, in myelofibrosis. N. Engl. J. Med. 363, 1117\u20131127 (2010).","journal-title":"N. Engl. J. Med"},{"key":"65673_CR22","doi-asserted-by":"crossref","unstructured":"Hoss, F., Rolfes, V., Davanso, M. R., Braga, T. T. & Franklin, B. S. Detection of ASC speck formation by flow cytometry and chemical cross-linking. in Innate Immune Activation (eds De Nardo, D. & De Nardo, C. M.) 1714 149\u2013165 (Springer New York, 2018).","DOI":"10.1007\/978-1-4939-7519-8_10"},{"key":"65673_CR23","doi-asserted-by":"publisher","first-page":"1464","DOI":"10.1182\/blood-2013-04-498956","volume":"122","author":"S Hasan","year":"2013","unstructured":"Hasan, S. et al. JAK2V617F expression in mice amplifies early hematopoietic cells and gives them a competitive advantage that is hampered by IFN\u03b1. Blood 122, 1464\u20131477 (2013).","journal-title":"Blood"},{"key":"65673_CR24","doi-asserted-by":"publisher","first-page":"132","DOI":"10.1016\/j.exphem.2015.10.008","volume":"44","author":"J Hoggatt","year":"2016","unstructured":"Hoggatt, J., Hoggatt, A. F., Tate, T. A., Fortman, J. & Pelus, L. M. Bleeding the laboratory mouse: Not all methods are equal. Exp. Hematol. 44, 132\u2013137.e1 (2016).","journal-title":"Exp. Hematol."},{"key":"65673_CR25","doi-asserted-by":"publisher","first-page":"143","DOI":"10.1034\/j.1600-0609.2001.00359.x","volume":"66","author":"MK Jensen","year":"2001","unstructured":"Jensen, M. K., De Nully Brown, P., Lund, B. V., Nielsen, O. J. & Hasselbalch, H. C. Increased circulating platelet-leukocyte aggregates in myeloproliferative disorders is correlated to previous thrombosis, platelet activation and platelet count: Platelet-leukocyte aggregates in myeloproliferative disorders. Eur. J. Haematol. 66, 143\u2013151 (2001).","journal-title":"Eur. J. Haematol."},{"key":"65673_CR26","doi-asserted-by":"publisher","first-page":"954","DOI":"10.1007\/s12015-020-10005-w","volume":"16","author":"M Adamiak","year":"2020","unstructured":"Adamiak, M. et al. Nlrp3 inflammasome signaling regulates the homing and engraftment of hematopoietic stem cells (HSPCs) by enhancing incorporation of CXCR4 receptor into membrane lipid rafts. Stem Cell Rev. Rep. 16, 954\u2013967 (2020).","journal-title":"Stem Cell Rev. Rep."},{"key":"65673_CR27","doi-asserted-by":"publisher","first-page":"1173","DOI":"10.1084\/jem.20091318","volume":"207","author":"Y Morita","year":"2010","unstructured":"Morita, Y., Ema, H. & Nakauchi, H. Heterogeneity and hierarchy within the most primitive hematopoietic stem cell compartment. J. Exp. Med. 207, 1173\u20131182 (2010).","journal-title":"J. Exp. Med."},{"key":"65673_CR28","doi-asserted-by":"publisher","first-page":"23","DOI":"10.1038\/ncb3346","volume":"18","author":"EM Pietras","year":"2016","unstructured":"Pietras, E. M. et al. Chronic interleukin-1 exposure drives haematopoietic stem cells towards precocious myeloid differentiation at the expense of self-renewal. Nat. Cell Biol. 18, 23 (2016).","journal-title":"Nat. Cell Biol."},{"key":"65673_CR29","doi-asserted-by":"publisher","first-page":"106","DOI":"10.1038\/nature25455","volume":"554","author":"J Carrelha","year":"2018","unstructured":"Carrelha, J. et al. Hierarchically related lineage-restricted fates of multipotent haematopoietic stem cells. Nature 554, 106\u2013111 (2018).","journal-title":"Nature"},{"key":"65673_CR30","doi-asserted-by":"publisher","DOI":"10.1038\/s41467-022-31914-z","volume":"13","author":"MNF Morcos","year":"2022","unstructured":"Morcos, M. N. F. et al. Fate mapping of hematopoietic stem cells reveals two pathways of native thrombopoiesis. Nat. Commun. 13, 4504 (2022).","journal-title":"Nat. Commun."},{"key":"65673_CR31","doi-asserted-by":"publisher","first-page":"212","DOI":"10.1038\/nature25168","volume":"553","author":"AE Rodriguez-Fraticelli","year":"2018","unstructured":"Rodriguez-Fraticelli, A. E. et al. Clonal analysis of lineage fate in native haematopoiesis. Nature 553, 212\u2013216 (2018).","journal-title":"Nature"},{"key":"65673_CR32","doi-asserted-by":"publisher","DOI":"10.1038\/s41598-019-40619-1","volume":"9","author":"OM Finucane","year":"2019","unstructured":"Finucane, O. M., Sugrue, J., Rubio-Araiz, A., Guillot-Sestier, M.-V. & Lynch, M. A. The NLRP3 inflammasome modulates glycolysis by increasing PFKFB3 in an IL-1\u03b2-dependent manner in macrophages. Sci. Rep. 9, 4034 (2019).","journal-title":"Sci. Rep."},{"key":"65673_CR33","doi-asserted-by":"publisher","first-page":"402","DOI":"10.1182\/blood.V88.2.402.bloodjournal882402","volume":"88","author":"X Yan","year":"1996","unstructured":"Yan, X. et al. A model of myelofibrosis and osteosclerosis in mice induced by overexpressing thrombopoietin (mpl ligand): reversal of disease by bone marrow transplantation. Blood 88, 402\u2013409 (1996).","journal-title":"Blood"},{"key":"65673_CR34","doi-asserted-by":"publisher","DOI":"10.1126\/sciadv.abd3139","volume":"6","author":"D Prins","year":"2020","unstructured":"Prins, D. et al. The stem\/progenitor landscape is reshaped in a mouse model of essential thrombocythemia and causes excess megakaryocyte production. Sci. Adv. 6, eabd3139 (2020).","journal-title":"Sci. Adv."},{"key":"65673_CR35","doi-asserted-by":"publisher","first-page":"477","DOI":"10.1016\/j.molcel.2020.04.008","volume":"78","author":"B Psaila","year":"2020","unstructured":"Psaila, B. et al. Single-cell analyses reveal megakaryocyte-biased hematopoiesis in myelofibrosis and identify mutant clone-specific targets. Mol. Cell 78, 477\u2013492.e8 (2020).","journal-title":"Mol. Cell"},{"key":"65673_CR36","doi-asserted-by":"publisher","first-page":"75","DOI":"10.1016\/j.lab.2003.09.006","volume":"143","author":"CKY Chuen","year":"2004","unstructured":"Chuen, C. K. Y. et al. Interleukin-1\u03b2 up-regulates the expression of thrombopoietin and transcription factors c-Jun, c-fos, GATA-1, and nf-E2 in megakaryocytic cells. J. Lab. Clin. Med. 143, 75\u201388 (2004).","journal-title":"J. Lab. Clin. Med."},{"key":"65673_CR37","doi-asserted-by":"publisher","DOI":"10.1172\/jci.insight.159430","volume":"7","author":"AF McLemore","year":"2022","unstructured":"McLemore, A. F. et al. Somatic gene mutations expose cytoplasmic DNA to co-opt the cGAS\/STING\/NLRP3 axis in myelodysplastic syndromes. JCI Insight 7, e159430 (2022).","journal-title":"JCI Insight"},{"key":"65673_CR38","doi-asserted-by":"publisher","first-page":"2","DOI":"10.1186\/s40164-016-0032-7","volume":"5","author":"EL Liew","year":"2015","unstructured":"Liew, E. L. et al. Identification of AIM2 as a downstream target of JAK2V617F. Exp. Hematol. Oncol. 5, 2 (2015).","journal-title":"Exp. Hematol. Oncol."},{"key":"65673_CR39","doi-asserted-by":"publisher","first-page":"1009","DOI":"10.1016\/j.immuni.2012.08.027","volume":"37","author":"SL Masters","year":"2012","unstructured":"Masters, S. L. et al. NLRP1 inflammasome activation induces pyroptosis of hematopoietic progenitor cells. Immunity 37, 1009\u20131023 (2012).","journal-title":"Immunity"},{"key":"65673_CR40","doi-asserted-by":"publisher","first-page":"334","DOI":"10.4049\/jimmunol.1202737","volume":"190","author":"Y He","year":"2013","unstructured":"He, Y., Franchi, L. & N\u00fa\u00f1ez, G. TLR agonists stimulate Nlrp3-dependent IL-1\u03b2 production independently of the purinergic P2X7 receptor in dendritic cells and in vivo. J. Immunol. 190, 334\u2013339 (2013).","journal-title":"J. Immunol."},{"key":"65673_CR41","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1016\/j.jim.2017.03.004","volume":"447","author":"M O\u2019Brien","year":"2017","unstructured":"O\u2019Brien, M. et al. A bioluminescent caspase-1 activity assay rapidly monitors inflammasome activation in cells. J. Immunol. Methods 447, 1\u201313 (2017).","journal-title":"J. Immunol. Methods"},{"key":"65673_CR42","doi-asserted-by":"publisher","first-page":"29","DOI":"10.1016\/j.ccell.2017.11.009","volume":"33","author":"M Kleppe","year":"2018","unstructured":"Kleppe, M. et al. Dual targeting of oncogenic activation and inflammatory signaling increases therapeutic efficacy in myeloproliferative neoplasms. Cancer Cell 33, 29\u201343.e7 (2018).","journal-title":"Cancer Cell"},{"key":"65673_CR43","doi-asserted-by":"publisher","first-page":"613","DOI":"10.4049\/jimmunol.1100613","volume":"187","author":"F Bauernfeind","year":"2011","unstructured":"Bauernfeind, F. et al. Cutting edge: reactive oxygen species inhibitors block priming, but not activation, of the NLRP3 inflammasome. J. Immunol. 187, 613\u2013617 (2011).","journal-title":"J. Immunol."},{"key":"65673_CR44","doi-asserted-by":"publisher","first-page":"162","DOI":"10.1016\/j.cell.2017.12.013","volume":"172","author":"A Christ","year":"2018","unstructured":"Christ, A. et al. Western diet triggers NLRP3-dependent innate immune reprogramming. Cell 172, 162\u2013175.e14 (2018).","journal-title":"Cell"},{"key":"65673_CR45","doi-asserted-by":"publisher","first-page":"995","DOI":"10.1038\/s41375-018-0295-6","volume":"33","author":"J Czech","year":"2019","unstructured":"Czech, J. et al. JAK2V617F but not CALR mutations confer increased molecular responses to interferon-\u03b1 via JAK1\/STAT1 activation. Leukemia 33, 995\u20131010 (2019).","journal-title":"Leukemia"},{"key":"65673_CR46","doi-asserted-by":"publisher","unstructured":"K\u00f6rber, R.-M., Saenz, L. M., Wolf, D. & Teichmann, L. Supplementary 3\u2019-mRNA sequencing dataset: Hematopoietic stem cells (HSC) and megakarocyte progenitors (MkP) from bone marrow of Jak2VF and Jak2VF;Nlrp3\u2212\/\u2212 mice. Zenodo https:\/\/doi.org\/10.5281\/ZENODO.16893730 (2025).","DOI":"10.5281\/ZENODO.16893730"}],"container-title":["Nature Communications"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.nature.com\/articles\/s41467-025-65673-4.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.nature.com\/articles\/s41467-025-65673-4","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.nature.com\/articles\/s41467-025-65673-4.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,11,26]],"date-time":"2025-11-26T14:04:22Z","timestamp":1764165862000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.nature.com\/articles\/s41467-025-65673-4"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2025,11,26]]},"references-count":46,"journal-issue":{"issue":"1","published-online":{"date-parts":[[2025,12]]}},"alternative-id":["65673"],"URL":"https:\/\/doi.org\/10.1038\/s41467-025-65673-4","relation":{"has-preprint":[{"id-type":"doi","id":"10.1101\/2024.03.09.583936","asserted-by":"object"}]},"ISSN":["2041-1723"],"issn-type":[{"value":"2041-1723","type":"electronic"}],"subject":[],"published":{"date-parts":[[2025,11,26]]},"assertion":[{"value":"14 March 2024","order":1,"name":"received","label":"Received","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"20 October 2025","order":2,"name":"accepted","label":"Accepted","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"26 November 2025","order":3,"name":"first_online","label":"First Online","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"R.M.K. received honoraria from Stemline. C.K. is an employee of AbbVie Deutschland GmbH & Co. KG. T.H.B. served as a consultant or invited speaker for Astra-Zeneca, Gilead, Janssen, Merck, Novartis and Pfizer and received research funding from Novartis and Pfizer. SK reports research grant\/funding from Geron, Janssen, AOP Pharma, and Novartis; consulting fees from Pfizer, Incyte, Ariad, Novartis, AOP Pharma, Bristol Myers Squibb, Celgene, Geron, Janssen, CTI BioPharma, Roche, Bayer, GSK, Sierra Oncology, and PharmaEssentia; payment or honoraria from Novartis, BMS\/Celgene, Pfizer; travel\/accommodation support from Alexion, Novartis, Bristol Myers Squibb, Incyte, AOP Pharma, CTI BioPharma, Pfizer, Celgene, Janssen, Geron, Roche, AbbVie, GSK, Sierra Oncology, and Karthos; a patent issued for a BET inhibitor at RWTH Aachen University; advisory board activity for from Pfizer, Incyte, Ariad, Novartis, AOP Pharma, BMS, Celgene, Geron, Janssen, CTI BioPharma, Roche, Bayer, GSK, Sierra Oncology, and PharmaEssentia. MG reports speaker bureau and consultancy for AOP Orphan, Celgene, CTI, Novartis, and Shire. I.G. received funding from aTyr. E.L. is co-founder and consultant to IFM Therapeutics, Odyssey Therapeutics and a Stealth Biotech company. D.W. served as a consultant or invited speaker for Novartis, Roche, BMS, Gilead, Janssen, MSD, AOP Orphan and Pfizer and received research funding from Novartis, BMS, AOP Orphan and Pfizer. L.L.T. reports honoraria from AOP Orphan, Boehringer Ingelheim, BMS and Novartis; consultancy for Astellas, Blueprint, BMS, GSK, Jazz Pharmaceuticals, Pfizer, and Sobi. The remaining authors declare no competing financial interests.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"10591"}}