AI Article Synopsis
- Type I interferon (IFN) induction is essential for the innate immune response against infections, but its effects on macrophages are not fully understood.
- Infection boosts the expression of IFN-β mRNA and triggers a signaling pathway involving STING, TBK1, and IRF3, leading to IFN-β production.
- Interestingly, while CARMA3 expression is stimulated during infection, it does not influence the phosphorylation of TBK1 or IRF3 in various cell types, indicating that IFN-β production occurs independently of CARMA3.
Article Abstract
Type I interferon (IFN) induction is a critical component of innate immune response to viral and bacterial infection, including , but whether it activates the signaling in macrophages and the regulation mechanisms is less well understood. Here we show that infection promoted the IFN-β mRNA expression and stimulator of IFN genes (STING)/TANK-binding kinase 1 (TBK1)/interferon regulatory factor 3 (IRF3)-dependent production of IFN-β. Infection with induced caspase recruitment domain and membrane-associated guanylate kinase-like domain protein 3 (CARMA3) expression at both the mRNA and protein levels. The heat-killed bacteria failed to trigger IRF3 phosphorylation and upregulation of CARMA3 expression. However, overexpression of CARMA3 did not affect phosphorylation of TBK1 or IRF3 in RAW264.7 cells, J774A.1 macrophages, and mouse embryonic fibroblast (MEF) cells. In conclusion, infection induces STING/TBK1/IRF3-mediated IFN-β production in a CARMA3-independent manner.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8000617 | PMC |
| http://dx.doi.org/10.3390/pathogens10030300 | DOI Listing |
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