Loss of MAPK-activated protein kinase 2 enables potent dendritic cell-driven anti-tumour T cell response.

ABSTRACT: Maintaining dendritic cells (DC) in a state of dysfunction represents a key mechanism by which tumour cells evade recognition and elimination by the immune system. Limited knowledge about the intracellular mediators of DC dysfunction restricts success of therapies aimed at reactivating a DC-driven anti-tumour immune response. Using a cell type-specific murine knock-out model, we have identified MAPK-activated protein kinase 2 (MK2) as a major guardian of a suppressive DC phenotype in the melanoma tumour microenvironment. MK2 deletion in CD11c⁺ cells led to an expansion of stimulatory CD103⁺ DCs, mounting a potent CD8⁺ T cell response that resulted in elimination of highly aggressive B16-F10 tumours upon toll-like receptor (TLR) activation in the presence of

SUBMITTER: Soukup K 

PROVIDER: S-EPMC5603533 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature