Figure 4.

Schematic model of AXL-mediated mechanisms of immune escape and the various facets of immunosenzitisation induced by targeting AXL. High AXL expression endows cancer cells with the ability to evade immune-mediated recognition and killing through multiple mechanisms. Cancer cells with active AXL signaling generally express more PD-L1 but less MHC class I molecules, ICAM-1, and NKG2D ligands than cells with inactive or reduced AXL signaling. These characteristics are associated with reduced recognition and elimination by cytotoxic lymphocytes. These cells also secrete an array of cytokines that attract immunosuppressive cell populations or directly inhibit cytotoxic immune cells, further limiting immune responses. Targeting AXL may partially reverse this phenomenon and sensitize carcinoma cells to immune attacks, while amplifying immune responses through the induction of immunogenic cell death.