Immunotherapy uses the body’s immune system to find and terminate cancerous cells, and has revolutionized cancer treatment. However, in certain cancers, such as lung cancer, less than 50% of patients respond to treatment. This is in part due to the immunosuppressive tumor microenvironment, which is composed of factors that promote tumor growth and proliferation. Tumor cells create a highly immunosuppressive microenvironment by triggering the anti-inflammatory phenotype of myeloid immune cells, which largely consist of tumor-associated macrophages (TAMs). Anti-PD-1 and anti-PD-L1 immune checkpoint blockade therapy helps promote the T cell anti-tumor response by releasing the brakes on cytotoxic T-cells. However, it is unclear how TAMs respond to these immune checkpoint antibodies. Our lab hypothesizes that blockade of the PD-1/PD-L1 signaling pathway drives a pro-inflammatory macrophage phenotype. This hypothesis is supported by data generated in the B16F10 murine melanoma model, but it is unknown whether macrophage response to PD-L1 blockade is generalizable to other tumor contexts. Thus, the goal of the project is to determine the impact of immune checkpoint blockade on murine macrophages in the Lewis Lung Carcinoma (LLC) model. Using Flow Cytometry, macrophage phenotypes will be analyzed to confirm whether a pro- inflammatory or anti-tumor response is generated.