Written thesis based on research on how A2A receptor stimulation can regulate intracellular proteins in macrophages. Main focus is on the interaction between A2A receptors and NPC1 protein in LPS-activated mouse peritoneal macrophages. NPC1 disease is a Lysosomal storage disorder that is characterized by intracellular accumulation of cholesterol and dysfunction of many cells, mainly macrophages, oligodendrocytes and hepatocytes. This thesis shows how A2A receptors and NPC1 protein have a functional relationship and when A2A receptors are stimulated and how it changes the translational, transcription, protein expression and localization in LPS-activated peritoneal macrophages. The results and its evaluation further strengthens our understanding of the functional relationship between A2A receptors on NPC1 protein.