Cachexia is a devastating syndrome with cardinal features of anorexia, weight loss, and fatigue. This syndrome occurs during numerous chronic diseases, such as cancer, cirrhosis, congestive heart failure, and rheumatoid arthritis. While mechanisms of cachexia are still not well understood, our lab and others demonstrated that inflammation within distinct brain regions can cause signs and symptoms similar to those observed during cachexia. Specifically, inflammation in the mediobasal hypothalamus can drive aberrant activation of the weight- and activity-mediating neurons in the region, causing decreased food intake, loss of skeletal muscle, and decreased locomotor activity. Mechanisms by which inflammation generated in the periphery is translated to inflammation in the brain have yet to be elucidated. Furthermore, cellular sources of neuroinflammation during cachexia are not known. The purpose of this dissertation was to identify and characterize the role of immune cells in the brain during cancer cachexia.