The abstract is read at the publisher; the summary is JClub's.
JAK STAT signaling is a convergent, potentially actionable cytokine axis in immune checkpoint inhibitor myocarditis, and it is amplified in clonal hematopoiesis carriers.
- Why it matters: Immune checkpoint inhibitor myocarditis affects up to 2% of patients and can have up to 50% mortality, and CHIP is a linked risk factor that may shape immune pathways and treatment resistance.
- What they did: In 236 cardio-oncology patients (88 on ICI), cytokines from ICI patients were profiled and analyzed with machine learning and explainable AI; single-cell multi-omics from Yale (n=19), Stanford (n=25), and MGH (n=63) assessed cell-type contributions, with Yale proteomics validated using Stanford CYTOF.
- The result: Features linked to ICI myocarditis included IL13, CXCL10, PDGFA, CCL13, CCL17, and KITlg, and single-cell consensus signals separating myocarditis from non-myocarditis were driven by module-level JAK STAT, T cell, and Toll like receptor activation, with CHIP carriers showing NF kappa B, IL17, MAPK, and TNF programs.
The findingWhy it mattersWhat they didThe result
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