Tumour rewires host tryptophan metabolism to promote organism-wide immune suppression
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How tumour genotype reshapes systemic metabolism to drive immune tolerance and tumour progression remains unclear. Here, we show that Pten -deficient Drosophila tumours reprogram host tryptophan metabolism, triggering systemic and local changes in immune compartments to foster tolerance. Tumour-derived nitric oxide activates the kynurenine pathway in liver-like tissue, selectively increasing the 3-hydroxykynurenine (3-HK) branch. Host 3-HK promotes tumour progression and suppresses immune function via aryl hydrocarbon receptor (AhR) signalling. These results identify the kynurenine pathway as a central tumour–host nexus and reveal how tumour genotype creates immune vulnerabilities.
