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. Author manuscript; available in PMC: 2024 Jun 19.
Published in final edited form as: Adv Immunol. 2024 May 3;161:53–83. doi: 10.1016/bs.ai.2024.03.001

Fig. 3. Intra-and extracellular self-ligands of PRRs leading to downstream effects in the brain.

Fig. 3

In the cytoplasm, expanded repeats, long 3′UTRs in mRNA, double-stranded mitochondrial RNAs (mtRNAs), and unedited transcripts can activate PKR and MDA5, stimulating inflammation, type I IFN production, and neuronal apoptosis triggered by translational shutdown. Cytoplasmic DNA and mitochondrial DNA (mtDNA) can stimulate cGAS and AIM2 activity to induce inflammation and pyroptosis. Extracellular miRNA, HERV-K, cell free dsRNA, mtDNA, and NETs can activate TLRs in neighboring cells leading to pain transmission, neuronal growth control, inflammation, and type I IFN production.