What is it about?

Here we show that T lymphocytes, previously thought to be exhausted by chronic exposure to the tumor mass, do not show marks of exhaustion. Instead T cells are held back by tumor cells by means of the interaction of two molecules named PD-1 and PD-L1. We show that Programmed cell death protein 1 or PD-1 is found on the T cell; its partner, the ligand PD-L1, is found on the lung tumor cells. When the pair is engaged, then the brake is on, T cells reduce the production of effector molecules and cannot attack the tumor cells. The use of an inhibitor for PD-L1 decouples the pairing and allow the T cell to recover the production of cytotoxic molecules.

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Why is it important?

In this study we demonstrate for the first time in lung cancer patients that rather than being exhausted and prone to dying, tumor-specific CD8+ T cells are reversibly held back by PD-L1. Thus, lung cancer patients may respond to checkpoint immunotherapy.

Perspectives

Here we propose a mechanism of how checkpoint immunotherapy based in anti-PD-L1 antibodies might work in lung cancer patients

Heriberto Prado-Garcia
Instituto Nacional de Enfermedades Respiratorias "Ismael Cosio Villegas"

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This page is a summary of: The PD-L1/PD-1 pathway promotes dysfunction, but not “exhaustion”, in tumor-responding T cells from pleural effusions in lung cancer patients, Cancer Immunology Immunotherapy, March 2017, Springer Science + Business Media, DOI: 10.1007/s00262-017-1979-x.
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