A mathematic model to reveal delicate cross-regulation between MAVS/STING, inflammasome and MyD88-dependent type I interferon signalling.

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

SUBMITTER: Cai C 

PROVIDER: S-EPMC7576308 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature