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Abstract Interleukin-10 (IL-10) is a central anti-inflammatory cytokine that suppresses immune responses in myeloid cells but can also activate T cells, limiting its therapeutic use in chronic inflammatory diseases owing to narrow efficacy windows and dose-limiting toxicities1,2,3,4,5. Here we show that myeloid and T cells differ in their dependence on JAK-family kinase pairing for IL-10 signalling and function.
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