The abstract is read at the publisher; the summary is JClub's.
IL-18 depletion in genetically engineered mice with spontaneous pancreatic ductal adenocarcinoma suppresses tumor progression and prolongs survival, linked to STAT1-dependent immune evasion.
- Why it matters: IL-18 is elevated in PDAC and correlates with poor outcomes, but its functional role in shaping immune regulation and cancer progression is not well defined.
- What they did: The study used IL-18-depleted genetically engineered mouse models, single-cell RNA-sequencing, and functional assays to assess macrophage phenotypes, STAT1 signaling, CD47 expression, and cancer–macrophage interactions.
- The result: IL-18 depletion reduced cancer cell survival and improved macrophage-mediated phagocytosis, enriching MHCII- and CD11c-positive antigen-presenting macrophages and enhancing KRAS inhibitor efficacy.
The findingWhy it mattersWhat they didThe result
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