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.

Featured Image

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.


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"

Read the Original

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.
You can read the full text:




The following have contributed to this page