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CXCR6 positions cytotoxic T cells to receive critical survival signals in the tumor microenvironment. | LitMetric

AI Article Synopsis

Article Abstract

Cytotoxic T lymphocyte (CTL) responses against tumors are maintained by stem-like memory cells that self-renew but also give rise to effector-like cells. The latter gradually lose their anti-tumor activity and acquire an epigenetically fixed, hypofunctional state, leading to tumor tolerance. Here, we show that the conversion of stem-like into effector-like CTLs involves a major chemotactic reprogramming that includes the upregulation of chemokine receptor CXCR6. This receptor positions effector-like CTLs in a discrete perivascular niche of the tumor stroma that is densely occupied by CCR7 dendritic cells (DCs) expressing the CXCR6 ligand CXCL16. CCR7 DCs also express and trans-present the survival cytokine interleukin-15 (IL-15). CXCR6 expression and IL-15 trans-presentation are critical for the survival and local expansion of effector-like CTLs in the tumor microenvironment to maximize their anti-tumor activity before progressing to irreversible dysfunction. These observations reveal a cellular and molecular checkpoint that determines the magnitude and outcome of anti-tumor immune responses.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8719451PMC
http://dx.doi.org/10.1016/j.cell.2021.07.015DOI Listing

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