The crosstalk between autophagy and myeloid-derived suppressor cell responses in cancer.

Abstract

The development of cancers is aided by the accumulation of myeloid-derived suppressor cells (MDSCs) within tumors, which are highly effective at suppressing anti-tumor immune responses. Direct cell-to-cell interaction and the production of immunosuppressive mediators have both been proposed as pathways for MDSC-mediated suppression of anti-tumor immune responses. The majority of current cancer treatments focus on altering the development and activity of MDSCs so that they have more of an immunogenic character. Autophagy is a catabolic system that contributes to the breakdown of damaged intracellular material and the recycling of metabolites. However, depending on the stage of tumor growth, autophagy can play both a prophylactic and a therapeutic function in carcinogenesis. However, several indirect lines of research have indicated that autophagy is a significant regulator of MDSC activity. The purpose of this work was to outline the interactions between MDSC and autophagy in cancer.