AI Article Synopsis
- The study investigates how cytosolic nucleic acids trigger immune responses via pattern recognition receptors like STING and RIG-I, leading to type I interferon production crucial for fighting viral infections.
- Researchers found that the DUSP4 phosphatase plays a significant role in regulating the immune signaling pathways by controlling the activation of key proteins TBK1 and ERK1/2, which are involved in type I interferon production.
- Mice lacking DUSP4 showed increased resistance to viral infections but were more vulnerable to malaria, highlighting DUSP4’s importance in managing immune responses to different pathogens.
Article Abstract
Detection of cytosolic nucleic acids by pattern recognition receptors, including STING and RIG-I, leads to the activation of multiple signalling pathways that culminate in the production of type I interferons (IFNs) which are vital for host survival during virus infection. In addition to protective immune modulatory functions, type I IFNs are also associated with autoimmune diseases. Hence, it is important to elucidate the mechanisms that govern their expression. In this study, we identified a critical regulatory function of the DUSP4 phosphatase in innate immune signalling. We found that DUSP4 regulates the activation of TBK1 and ERK1/2 in a signalling complex containing DUSP4, TBK1, ERK1/2 and IRF3 to regulate the production of type I IFNs. Mice deficient in DUSP4 were more resistant to infections by both RNA and DNA viruses but more susceptible to malaria parasites. Therefore, our study establishes DUSP4 as a regulator of nucleic acid sensor signalling and sheds light on an important facet of the type I IFN regulatory system.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10923883 | PMC |
| http://dx.doi.org/10.1038/s41418-024-01269-7 | DOI Listing |
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