Human immune cells must respond to very specific cues in the body by adhering to surfaces and spreading in a controlled manner. For instance, near a site of injury or infection, white blood cells detect certain molecules on the cells that line blood vessels, then proceed to adhere to these cells, spread, and squeeze out of the vessel into the surrounding tissue. Specialized white blood cells are capable of a unique type of cell spreading, phagocytosis. In phagocytosis, the cell adheres to a pathogen such as a fungus or a bacterium, then spreads around and completely engulfs the foreign entity. In my work, I study the physical forces and chemical signals involved when the most abundant type of white blood cell, the neutrophil, recognizes and engulfs different types of pathogenic particles. I use a combination of experiments and computational modeling to develop a fundamental understanding of phagocytosis, which could contribute essential knowledge for the development of future diagnostics or immunotherapies. In my experiments, I observe neutrophil phagocytosis using two setups. In the first, I use small glass tubes, known as a micropipettes, to hold a neutrophil and a pathogenic particle. I then bring the particle into contact with the cell and observe the cell’s phagocytic response. In the alternative setup, I coat an entire surface with molecules which commonly tag pathogens in the body (e.g. antibodies), drop neutrophils onto this surface, and observe subsequent cell spreading. In either experiment, I can carefully monitor changes in cell shape over time while also measuring changes in calcium concentration within the cell. I examine how the dynamics of phagocytosis and increases in intracellular calcium depend on the type of pathogenic surface and the density of adhesion molecules. Our lab recently found that the speed of cell spreading during phagocytosis does not change significantly when using higher densities of adhesion molecules on pathogenic surface, a surprising result we explored further via computational modeling. My computational models demonstrated that the forces driving neutrophil movement must be those actively exerted by the cell, rather than passive forces due to adhesion between cell membrane receptors and molecules on the surface.