MerTK Induces Dysfunctional Dendritic Cells by Metabolic Reprogramming.

ABSTRACT: Checkpoint inhibitors, specifically anti-programmed cell death protein 1 (PD1), have shown success in treating metastatic melanoma; however, some patients develop resistance. Dendritic cells (DC) play a key role in initiating an immune response, but in certain circumstances they become ineffective. We investigated the role of MerTK, a receptor tyrosine kinase responsible for myeloid cell clearance of dead cells, in the regulation of DC function and metabolism in the tumor microenvironment. Tumors resistant to anti-PD1 exhibited increased levels of MerTK+ DCs. Treating wild-type DCs with apoptotic melanoma cells in vitro resulted in increased MerTK expression, elevated mitochondrial respiration and fatty acid oxidation, and reduced T-cell stimulatory capacity, all characteristics of dysfunc

SUBMITTER: Zewdie EY 

PROVIDER: S-EPMC11371516 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature