The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that functions as an environmental sensor. It is classically thought to reside in the cytoplasm of cells when unbound but emerging evidence suggests that a pool of AHR is also located in the intermembrane space of mitochondria, termed mito-AHR. Ligands for the AHR, such as 2,3,7,8-tetrachlorodibenzo-ρ-dioxin (TCDD), have been shown to cause immune suppression by altering the activation of multiple cell types involved in the inflammatory process. Preliminary evidence from this lab has found that the level of AHR increases in the mitochondria of M1/M2 activated microglial cells, which are the specialized macrophages of the central nervous system. The goal of this thesis project will be to determine the role of mito-AHR during the activation of microglia. This will be assessed by (1) characterizing the localization of the AHR to the mitochondria during activation, (2) determining if mito-AHR is necessary for M1 and/or M2 activation, and (3) analyzing if mito-AHR functions in modulating mitochondrial function, including energetics and reactive species generation, during microglial activation. This project hopes to give more insight into the wider role of the AHR during immune responses.