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Here, we show that under physiological conditions, inactivation of ISG15, an inflammation amplifier, is associated with the interaction of Beclin 1 (Becn1), via its evolutionarily conserved domain, with STAT3 in the major fetal hematopoietic organ of mice. Conditional loss of\n                    <jats:italic>Becn1<\/jats:italic>\n                    caused sequential dysfunction and exhaustion of fetal liver hematopoietic stem cells, leading to lethal inflammatory cell\u2013biased hematopoiesis in the fetus. Molecularly, the absence of\n                    <jats:italic>Becn1<\/jats:italic>\n                    resulted in the release of STAT3 from Becn1 tethering and subsequent phosphorylation and translocation to the nucleus, which in turn directly activated the transcription of\n                    <jats:italic>ISG15<\/jats:italic>\n                    in fetal liver hematopoietic cells, coupled with increased ISGylation and production of inflammatory cytokines, whereas inactivating STAT3 reduced\n                    <jats:italic>ISG15<\/jats:italic>\n                    transcription and inflammation but improved hematopoiesis potential, and further silencing\n                    <jats:italic>ISG15<\/jats:italic>\n                    mitigated the above collapse in the\n                    <jats:italic>Becn1<\/jats:italic>\n                    -null hematopoietic lineage. The Becn1\/STAT3\/ISG15 axis remains functional in autophagy-disrupted fetal hematopoietic organs. These results suggest that Becn1, in an autophagy-independent manner, secures hematopoiesis and survival of the fetus by directly inhibiting STAT3\/ISG15 activation to prevent cytokine storms. Our findings highlight a previously undocumented role of Becn1 in governing ISG15 to safeguard the fetus.\n                  <\/jats:p>","DOI":"10.1172\/jci177375","type":"journal-article","created":{"date-parts":[[2024,11,26]],"date-time":"2024-11-26T12:00:56Z","timestamp":1732622456000},"source":"Crossref","is-referenced-by-count":5,"title":["Beclin 1 prevents ISG15-mediated cytokine storms to secure fetal hematopoiesis and survival"],"prefix":"10.1172","volume":"135","author":[{"given":"Wen","family":"Wei","sequence":"first","affiliation":[{"name":"Research Center for Blood Engineering and Manufacturing, Cyrus Tang Medical Institute, Soochow University, Suzhou, China."},{"name":"National Clinical Research Center for Hematologic Diseases, Key Laboratory of Thrombosis and Hemostasis Ministry of Health, Collaborative Innovation Center of Hematology, Jiangsu Institute of Hematology, Institute of Blood and Marrow Transplantation, The First Affiliated Hospital of Soochow University, 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