<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cai C</submitter><funding>National Natural Science Foundation of China</funding><pagination>11535-11545</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7576308</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(19)</volume><pubmed_abstract>Early type I interferon is essential for antagonizing against malaria infection, which remains a significant global infectious disease. After Plasmodium yoelii YM infection, the activation of MAVS-, STING- and inflammasome-IRF3-mediated pathway could trigger the Socs1 expression to inhibit the TLR7-MyD88-IRF7-induced type I interferon production. However, the dynamic regulatory mechanisms of type I interferon response to YM infection and delicate cross-regulation of these signalling are far from clear. In current study, we established a mathematical model to systematically demonstrate that the MAVS-, STING- and inflammasome-mediated signalling pathways play distinct roles in regulating type I interferon response after YM infection; and the YM dose could significantly affect the difference </pubmed_abstract><journal>Journal of cellular and molecular medicine</journal><pubmed_title>A mathematic model to reveal delicate cross-regulation between MAVS/STING, inflammasome and MyD88-dependent type I interferon signalling.</pubmed_title><pmcid>PMC7576308</pmcid><funding_grant_id>81960292</funding_grant_id><funding_grant_id>81801579</funding_grant_id><pubmed_authors>Cai C</pubmed_authors><pubmed_authors>Yu X</pubmed_authors></additional><is_claimable>false</is_claimable><name>A mathematic model to reveal delicate cross-regulation between MAVS/STING, inflammasome and MyD88-dependent type I interferon signalling.</name><description>Early type I interferon is essential for antagonizing against malaria infection, which remains a significant global infectious disease. After Plasmodium yoelii YM infection, the activation of MAVS-, STING- and inflammasome-IRF3-mediated pathway could trigger the Socs1 expression to inhibit the TLR7-MyD88-IRF7-induced type I interferon production. However, the dynamic regulatory mechanisms of type I interferon response to YM infection and delicate cross-regulation of these signalling are far from clear. In current study, we established a mathematical model to systematically demonstrate that the MAVS-, STING- and inflammasome-mediated signalling pathways play distinct roles in regulating type I interferon response after YM infection; and the YM dose could significantly affect the difference </description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Oct</publication><modification>2025-04-18T20:45:16.265Z</modification><creation>2020-10-29T14:51:48Z</creation></dates><accession>S-EPMC7576308</accession><cross_references><pubmed>32885594</pubmed><doi>10.1111/jcmm.15768</doi></cross_references></HashMap>