Phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF induces IRF3 activation

TLDR

Innate immune receptors such as RIG‑I, cGAS, and TLRs detect microbial fragments and signal through distinct adaptor proteins that activate TBK1 and IRF3 to induce interferon production, a process tightly regulated to prevent excessive inflammation. The study identifies a shared mechanism among RIG‑I, cGAS, and TLR adaptor proteins that activates IRF3 and drives interferon production. Published in Science (10.1126/science.aaa2630) by Liu et al.

Abstract

Innate immune receptor signaling, united Innate immune receptors such as RIG-I, cGAS, and Toll-like receptors bind microbial fragments and alert the immune system to an infection. Each receptor type signals through a different adapter protein. These signals activate the protein kinase TBK1 and the transcription factor IRF3, which tells cells to secrete interferon proteins (IFNs) important for host defense. Liu et al. now report a common signaling mechanism used by all three types of innate immune receptor-adaptor protein pairs to activate IRF3 and generate IFNs. This is important because cells must regulate their IFN production carefully to avoid inflammation and autoimmunity. Science , this issue 10.1126/science.aaa2630