Autoimmunity is the clinical manifestations of loss of tolerance to self antigens. While research efforts have so far focused on the effector phase of autoimmunity, we are interested in investigating the breaking of tolerance during the initiation phase. Thus, we use a mouse model of multiple sclerosis, Experimental Autoimmune Encephalomyelitis (EAE), in order to understand how environmental and genetic risk factors interact in triggering autoimmunity. We are interested in studying the role of Pattern Recognition Receptors (PRR) as the first line of recognition of stimuli that contribute to development of autoimmunity. PRR recognize stimuli originated both from pathogenic infections and endogenous ligands resulting from cellular metabolism and death. We have generated in-house knockout mouse lines to better understand which pathways are important in development of EAE. Due to our global approach, we started by characterizing clinical progression in each of the knockout mouse lines and generated disease progression and FACS data.