Engineered TYK2 dependence enables myeloid-selective IL-10 receptor agonism - Nature
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MainIL-10 is a potent anti-inflammatory cytokine that maintains immune tolerance1,6. Loss-of-function mutations in IL10 or its receptors IL10RA (encoding IL-10Rα) and IL10RB (encoding IL-10Rβ) cause early-onset inflammatory bowel disease (IBD) and autoinflammatory disorders1,7. IL-10 signalling is initiated when IL-10 binds to IL-10Rα and IL-10Rβ to form a tetrameric receptor complex, which is constitutively associated with Janus kinase 1 (JAK1) and tyrosine kinase 2 (TYK2), respectively1,8. This binding triggers JAK1-dependent phosphorylation of IL-10Rα and signal transducer and activator of transcription 3 (STAT3) to suppress pro-inflammatory gene expression and promote immune tolerance8,9. IL-10 primarily exerts its tolerogenic effects in myeloid cells and antigen-presenting cells, such as dendritic cells (DCs) and macrophages, by inhibiting cytokine production, antigen presentation and T cell priming5,10,11,12,13. Loss of IL10RA or STAT3 in these cells leads to colitis and systemic inflammation10,12,13. Despite its central role in immune tolerance, the dual functionality of IL-10 severely limits its therapeutic use6,14.
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