Around 5% of the western population are affected by inflammatory autoimmune diseases and often suffer under devastating consequences. A hallmark of these disorders is that tissue destruction is caused by the patient’s own immune system. Among these diseases multiple sclerosis is an autoimmune disease that affects the central nervous system and is the most frequent cause of non-reversible disabilities in young adults. A decisive step in the onset of inflammatory autoimmune diseases is the priming of an uncontrollable inflammatory pathogenic T cell response and the breakdown of immune homeostasis. Interestingly, increased levels of reactive oxygen species (ROS) are often found in inflammatory diseases indicating a disturbed cellular redox state in the disease context. The regulation of redox levels is fundamental to maintaining normal cellular functions and ensuring cellular homeostasis. Oxidative stress is derived from an imbalance between the generation and elimination of reactive oxygen species (ROS). Our project aims to evaluate the possibility of an anti-inflammatory treatment strategy by interfering with ROS signaling mainly in T cells. By a combination of genetic and pharmacological approaches in mice we will target redox homeostasis in the context of disease models that are relevant for human autoimmune diseases, in particular for multiple sclerosis. In parallel we evaluate the effects of our interference on a physiological anti-viral response. We will characterize T cell intrinsic signaling pathways and events that are relevant for autoimmune disease establishment or resistant and compare them to signaling events that are crucial for a physiological important anti-viral response. We aim to filter out signaling pathways that are most relevant for detrimental autoreactive, but of minor importance for protective anti-viral T cell responses in vivo. These pathways might serve as important targets for future disease interference with minor dampening of a physiological immune response.