A mathematic model to reveal delicate cross‐regulation between MAVS/STING, inflammasome and MyD88‐dependent type I interferon signalling
العنوان: | A mathematic model to reveal delicate cross‐regulation between MAVS/STING, inflammasome and MyD88‐dependent type I interferon signalling |
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المؤلفون: | Xiao Yu, Chunmei Cai |
المصدر: | Journal of Cellular and Molecular Medicine |
بيانات النشر: | John Wiley and Sons Inc., 2020. |
سنة النشر: | 2020 |
مصطلحات موضوعية: | 0301 basic medicine, Time Factors, Inflammasomes, malaria, Models, Biological, 03 medical and health sciences, 0302 clinical medicine, Suppressor of Cytokine Signaling 1 Protein, Interferon, medicine, Animals, Adaptor Proteins, Signal Transducing, Disease Resistance, biology, Suppressor of cytokine signaling 1, Membrane Proteins, Inflammasome, Cell Biology, Original Articles, Plasmodium yoelii, delicate cross‐regulation, Type I interferon production, biology.organism_classification, Cell biology, Mice, Inbred C57BL, Sting, 030104 developmental biology, Signalling, Infectious disease (medical specialty), 030220 oncology & carcinogenesis, Interferon Type I, Myeloid Differentiation Factor 88, Molecular Medicine, type I interferon, Original Article, Female, mathematical model, medicine.drug, Signal Transduction |
الوصف: | 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 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. |
اللغة: | English |
تدمد: | 1582-4934 1582-1838 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6d2141e70ec7159d803191e10a119778Test http://europepmc.org/articles/PMC7576308Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....6d2141e70ec7159d803191e10a119778 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15824934 15821838 |
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