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Here, we show that Src homology 2 containing inositol phosphatase 1 (SHIP1) suppresses IFN-I signaling by promoting IRF3 degradation during malaria infection. Genetic ablation of\n            <jats:italic>Ship1<\/jats:italic>\n            in mice leads to high levels of IFN-I and confers resistance to\n            <jats:italic>Plasmodium yoelii nigeriensis<\/jats:italic>\n            (\n            <jats:italic>P.y.<\/jats:italic>\n            ) N67 infection. Mechanistically, SHIP1 promotes the selective autophagic degradation of IRF3 by enhancing K63-linked ubiquitination of IRF3 at lysine 313, which serves as a recognition signal for NDP52-mediated selective autophagic degradation. In addition, SHIP1 is downregulated by IFN-I-induced miR-155-5p upon\n            <jats:italic>P.y<\/jats:italic>\n            . N67 infection and severs as a feedback loop of the signaling crosstalk. This study reveals a regulatory mechanism between IFN-I signaling and autophagy, and verifies SHIP1 can be a potential target for therapeutic intervention against malaria and other infectious diseases.\n          <\/jats:p>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              Malaria remains a serious disease affecting millions of people worldwide. Malaria parasite infection triggers tightly controlled type I interferon (IFN-I) signaling that plays a critical role in host innate immunity; however, the molecular mechanisms underlying the immune responses are still elusive. Here, we discover a host gene [Src homology 2-containing inositol phosphatase 1 (SHIP1)] that can regulate IFN-I signaling by modulating NDP52-mediated selective autophagic degradation of IRF3 and significantly affect parasitemia and resistance of\n              <jats:italic>Plasmodium<\/jats:italic>\n              -infected mice. This study identifies SHIP1 as a potential target for immunotherapies in malaria and highlights the crosstalk between IFN-I signaling and autophagy in preventing related infectious diseases. SHIP1 functions as a negative regulator during malaria infection by targeting IRF3 for autophagic degradation.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/mbio.03512-22","type":"journal-article","created":{"date-parts":[[2023,6,27]],"date-time":"2023-06-27T13:00:53Z","timestamp":1687870853000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":6,"title":["SHIP1 modulates antimalarial immunity by bridging the crosstalk between type I IFN signaling and autophagy"],"prefix":"10.1128","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1784-4595","authenticated-orcid":true,"given":"Hongyu","family":"Li","sequence":"first","affiliation":[{"name":"Department of Immunology, School of Basic Medical Sciences, Southern Medical University , Guangzhou, Guangdong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuai","family":"Yang","sequence":"additional","affiliation":[{"name":"Guangdong 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