{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T14:56:03Z","timestamp":1790607363708,"version":"4.1.0"},"reference-count":68,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2022,1,27]],"date-time":"2022-01-27T00:00:00Z","timestamp":1643241600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2022,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:italic>Toxoplasma gondii<\/jats:italic>\n                    is an opportunistic protozoan, which widely infects humans and other warm\u2010blooded animals. The type I interferon (IFN) such as IFN\u2010\u03b1\/\u03b2 is involved in cGAS\u2010STING signaling to resist\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>gondii<\/jats:italic>\n                    infection. We found in RAW264.7 cells, that\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>gondii<\/jats:italic>\n                    virulence factor\n                    <jats:italic>Tg<\/jats:italic>\n                    ROP18\n                    <jats:sub>I<\/jats:sub>\n                    , inhibited IFN\u2010\u03b2 production through interacting with interferon regulatory factor 3 (IRF3). Besides,\n                    <jats:italic>Tg<\/jats:italic>\n                    ROP18\n                    <jats:sub>I<\/jats:sub>\n                    interacted with p62 and Tumor Necrotic Factor Receptor Associated Factor 6 (TRAF6), which resulted in the inhibition of TRAF6\u2010p62 interaction, and phosphorylation of p62. Furthermore,\n                    <jats:italic>Tg<\/jats:italic>\n                    ROP18\n                    <jats:sub>I<\/jats:sub>\n                    restricted the recruitment of ubiquitin, p62 and microtubule\u2010associated protein light chain 3 (LC3) to the parasitophorous vacuole membrane (PVM) in IFN\u2010\u03b3\u2010stimulated murine cell line L929 cells. In IFN\u2010\u03b3\u2010stimulated human cells,\n                    <jats:italic>Tg<\/jats:italic>\n                    ROP18\n                    <jats:sub>I<\/jats:sub>\n                    restricted the decoration of PVM with ubiquitin, p62, and LC3, and bound with TRAF2, TRAF6, and p62, respectively. As a result,\n                    <jats:italic>Tg<\/jats:italic>\n                    ROP18\n                    <jats:sub>I<\/jats:sub>\n                    led to a successful parasitic replication in murine and human cells. Collectively, our study revealed the function of\n                    <jats:italic>Tg<\/jats:italic>\n                    ROP18\n                    <jats:sub>I<\/jats:sub>\n                    in suppressing host type I interferon responses in\n                    <jats:italic>T<\/jats:italic>\n                    .\n                    <jats:italic>gondii<\/jats:italic>\n                    infection for parasitic immune escape.\n                  <\/jats:p>","DOI":"10.1096\/fj.202101347r","type":"journal-article","created":{"date-parts":[[2022,1,27]],"date-time":"2022-01-27T11:29:21Z","timestamp":1643282961000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["<i>Toxoplasma gondii<\/i>\n                    ROP18\n                    <sub>I<\/sub>\n                    inhibits host innate immunity through cGAS\u2010STING signaling"],"prefix":"10.1096","volume":"36","author":[{"given":"Min","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Pathogen Biology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health Southern Medical University  Guangzhou P. 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