deletion enhances cross-priming of CD8+ T cells by tumor-infiltrating CD11b+ dendritic cells.

Background: Tumor-associated myeloid cells (TAMCs) are an abundant, phenotypically plastic cell population that is critical for initiating a robust antitumor response. To properly combat cancer cells, TAMCs must sense and transduce both soluble and vital biophysical cues imparted by the dense extracellular matrix (ECM) of the tumor microenvironment (TME). Despite ample research enumerating the deleterious effects of a primary tumor's ECM on TAMCs' functionality, few studies have evaluated the contribution of mechanosensitive cation channel(s) underlying these detrimental changes.