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Paucity of PD-L1 expression in prostate cancer: innate and adaptive immune resistance
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Paucity of PD-L1 expression in prostate cancer: innate and adaptive immune resistance
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Journal Article
Paucity of PD-L1 expression in prostate cancer: innate and adaptive immune resistance
2015
Overview
BACKGROUND:
Primary prostate cancers are infiltrated with programmed death-1 (PD-1) expressing CD8+ T-cells. However, in early clinical trials, men with metastatic castrate-resistant prostate cancer did not respond to PD-1 blockade as a monotherapy. One explanation for this unresponsiveness could be that prostate tumors generally do not express programmed death ligand-1 (PD-L1), the primary ligand for PD-1. However, lack of PD-L1 expression in prostate cancer would be surprising, given that phosphatase and tensin homolog (PTEN) loss is relatively common in prostate cancer and several studies have shown that PTEN loss correlates with PD-L1 upregulation—constituting a mechanism of innate immune resistance. This study tested whether prostate cancer cells were capable of expressing PD-L1, and whether the rare PD-L1 expression that occurs in human specimens correlates with PTEN loss.
METHODS:
Human prostate cancer cell lines were evaluated for PD-L1 expression and loss of PTEN by flow cytometry and western blotting, respectively. Immunohistochemical (IHC) staining for PTEN was correlated with PD-L1 IHC using a series of resected human prostate cancer samples.
RESULTS:
In vitro
, many prostate cancer cell lines upregulated PD-L1 expression in response to inflammatory cytokines, consistent with adaptive immune resistance. In these cell lines, no association between PTEN loss and PD-L1 expression was apparent. In primary prostate tumors, PD-L1 expression was rare, and was not associated with PTEN loss.
CONCLUSIONS:
These studies show that some prostate cancer cell lines are capable of expressing PD-L1. However, in human prostate cancer, PTEN loss is not associated with PD-L1 expression, arguing against innate immune resistance as a mechanism that mitigates antitumor immune responses in this disease.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/51
/ 82/80
/ Adaptive Immunity - genetics
/ Analysis
/ Antineoplastic Agents - pharmacology
/ Biomedical and Life Sciences
/ Complications and side effects
/ Gene Expression Regulation, Neoplastic - drug effects
/ Homology
/ Humans
/ Interferon-gamma - metabolism
/ Interferon-gamma - pharmacology
/ Ligands
/ Male
/ Prostatic Neoplasms - immunology
/ Prostatic Neoplasms - metabolism
/ Prostatic Neoplasms - pathology
/ PTEN Phosphohydrolase - genetics
/ PTEN Phosphohydrolase - metabolism
/ T cells
/ Tensin
/ Tosyl Compounds - pharmacology
/ Tumors
