Induction of NKG2D Ligands on Solid Tumors Requires Tumor-Specific CD8⁺ T Cells and Histone Acetyltransferases.

ABSTRACT: NKG2D-mediated immune surveillance is crucial for inhibiting tumor growth and metastases. Malignant tumor cells often downregulate NKG2D ligands to escape from immune surveillance. High-profile studies have shown that restoring NKG2D ligand expression via genetic engineering inhibits tumor formation and progression. However, no effective in vivo approaches are available to restore these ligands across different types of solid tumors because the classic stress signal-dependent induction of this ligand in vitro is transient and has rarely been duplicated in solid tumors in vivo We found that coadministration of an immune stimulatory signal (IL12) and chemotherapy (doxorubicin) restored the NKG2D ligand Rae-1 in multiple tumor types, including a human tumor model. The res

SUBMITTER: Hu J 

PROVIDER: S-EPMC5382872 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature