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A GPCR checkpoint drives CD8+ T cell dysfunction and immunotherapy failure in mice - Nature Immunology
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Tumor cells exploit G-protein-coupled receptor (GPCR) signaling networks to promote angiogenesis, grow and metastasize. We show that tumor cells leverage a GPCR–Gαs–protein kinase A (PKA) signaling axis to polarize CD8+ T cells into a dysfunctional state, thereby limiting the tumor infiltration and cytotoxic function of these cells and reducing the efficacy of current immunotherapies.
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