Mediator complex subunit MED23 dampens antiviral innate immunity by restricting RIG-I expression.

ABSTRACT: The detection of cytosolic viral nucleic acids via pattern-recognition receptors (PRRs) activates multiple signaling pathways, leading to the production of interferons (IFNs), which are essential for host survival during viral infection. Precise control of PRR gene expression is crucial for maintaining immune homeostasis. Here, we showed that Mediator complex subunit 23 (Med23) is required for the precise production of the innate immune receptor RIG-I in response to RNA virus infection. Med23 deficiency markedly enhances the production of IFN-I, proinflammatory cytokines, and IFN-stimulated genes (ISGs) in both multiple cell lines (MEFs, RAW264.7 cells, and HeLa cells) and mouse primary macrophages (bone marrow-derived macrophages [BMDMs] and peritoneal macrophages [PEMs]) infected with RN

SUBMITTER: Xiong DF 

PROVIDER: S-EPMC12316392 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature