IDH mutant gliomas escape natural killer cell immune surveillance by downregulation of NKG2D ligand expression.

ABSTRACT:

Background

Diffuse gliomas are poorly immunogenic, fatal brain tumors. The basis for insufficient antitumor immunity in diffuse gliomas is unknown. Gain-of-function mutations in isocitrate dehydrogenases (IDH1 and IDH2) promote diffuse glioma formation through epigenetic reprogramming of a number of genes, including immune-related genes. Here, we identify epigenetic dysregulation of natural killer (NK) cell ligand genes as significant contributors to immune escape in glioma.

Methods

We analyzed the database of The Cancer Genome Atlas for immune gene expression patterns in IDH mutant or wild-type gliomas and identified differentially expressed immune genes. NKG2D ligand expression levels and NK cell-mediated lysis were measured in IDH mutant and wild-type patient-derived glio

SUBMITTER: Zhang X 

PROVIDER: S-EPMC5035522 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature