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Interleukin-10 (IL-10) is a pleiotropic immunoregulatory cytokine, classically defined as a potent anti-inflammatory cytokine that protects tissues by constraining myeloid activation and limiting inflammatory cytokine production. In defined contexts it can also promote antitumour immunity by enhancing the fitness and cytotoxic programs of CD8+ T cells and NK cells, whereas in other tumour contexts the same pathway reinforces immunosuppressive myeloid and regulatory programs. Its effects converge on a common JAK1/TYK2–STAT3 signalling hub, but the downstream outcome is shaped combinatorially by co-engaged pathways (STAT1, STAT5, mTORC1, NF-κB/AP-1), IL-10 receptor abundance, feedback regulation and the chromatin state of the responding cell.
Interleukin-10 (IL-10) is a pleiotropic immunoregulatory cytokine, classically defined as a potent anti-inflammatory cytokine that protects tissues by constraining myeloid activation and limiting inflammatory cytokine production. In defined contexts it can also promote antitumour immunity by enhancing the fitness and cytotoxic programs of CD8+ T cells and NK cells, whereas in other tumour contexts the same pathway reinforces immunosuppressive myeloid and regulatory programs. Its effects converge on a common JAK1/TYK2–STAT3 signalling hub, but the downstream outcome is shaped combinatorially by co-engaged pathways (STAT1, STAT5, mTORC1, NF-κB/AP-1), IL-10 receptor abundance, feedback regulation and the chromatin state of the responding cell.
IL-10 signals through a heterohexameric receptor complex composed of one IL-10 homodimer, two high-affinity IL-10Rα (IL-10RA/CD210a) chains and two accessory IL-10Rβ (IL-10RB/CD210b) chains. Ligand binding juxtaposes the receptor-associated kinases JAK1 (bound to IL-10Rα) and TYK2 (bound to IL-10Rβ), enabling their mutual activation and initiating downstream JAK–STAT signalling; activated JAK1/TYK2 phosphorylate the IL-10Rα cytoplasmic tail, creating docking sites for STAT proteins. STAT3 is the dominant effector, although STAT1 can also be engaged in a context-dependent manner. Signalling amplitude and duration are limited by negative feedback (induction of SOCS3/SOCS1, dephosphorylation by SHP-1, receptor ubiquitination/downregulation), and the biological outcome is determined combinatorially by the receptor chains and kinases engaged, parallel pathways (STAT1, STAT5, mTORC1, NF-κB/AP-1), receptor abundance and the chromatin state of the responding cell.
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