{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T11:03:56Z","timestamp":1771412636559,"version":"3.50.1"},"reference-count":42,"publisher":"Wiley","issue":"19","license":[{"start":{"date-parts":[[2020,9,3]],"date-time":"2020-09-03T00:00:00Z","timestamp":1599091200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2020,9,3]],"date-time":"2020-09-03T00:00:00Z","timestamp":1599091200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81960292"],"award-info":[{"award-number":["81960292"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81801579"],"award-info":[{"award-number":["81801579"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2020,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Early type I interferon is essential for antagonizing against malaria infection, which remains a significant global infectious disease. After\n                    <jats:italic>Plasmodium yoelii<\/jats:italic>\n                    YM infection, the activation of MAVS\u2010, STING\u2010 and inflammasome\u2010IRF3\u2010mediated pathway could trigger the\n                    <jats:italic>Socs1<\/jats:italic>\n                    expression to inhibit the TLR7\u2010MyD88\u2010IRF7\u2010induced type I interferon production. However, the dynamic regulatory mechanisms of type I interferon response to YM infection and delicate cross\u2010regulation of these signalling are far from clear. In current study, we established a mathematical model to systematically demonstrate that the MAVS\u2010, STING\u2010 and inflammasome\u2010mediated signalling pathways play distinct roles in regulating type I interferon response after YM infection; and the YM dose could significantly affect the difference of resistance to YM infection among MAVS, STING and inflammasome deficiency. Collectively, our study systematically elucidated the precise regulatory mechanisms of type I interferon signalling after YM infection and advanced the research on therapy of plasmodium infection by incorporating multiple signalling pathways at diverse time.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.15768","type":"journal-article","created":{"date-parts":[[2020,9,3]],"date-time":"2020-09-03T23:49:36Z","timestamp":1599176976000},"page":"11535-11545","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["A mathematic model to reveal delicate cross\u2010regulation between MAVS\/STING, inflammasome and MyD88\u2010dependent type I interferon signalling"],"prefix":"10.1111","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6984-4637","authenticated-orcid":false,"given":"Chunmei","family":"Cai","sequence":"first","affiliation":[{"name":"Research Center for High Altitude Medicine School of Medical 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