Multiple sclerosis (MS) is a neurodegenerative disease which causes numbness, paralysis, pain and fatigue as a result of the body's immune system attacking the central nervous system (CNS). Diagnosis occurs between the ages of 20 and 50 and disproportionately affects women and people of Northern European descent. This disease affects approximately 2.8 million people worldwide, and even with treatment, shortens life expectancy by approximately seven years (Walton et al.). Many risk factors have been identified and immunotherapies developed, but no specific cure or definitive cause has been found. The current immunotherapies used for MS target the entire immune system and can have significant immunocompromising side effects (Rafiee et al).To model MS and investigate the cells contributing to autoimmunity, we use the murine model, Experimental Autoimmune Encephalomyelitis (EAE). Per this model, following delivery of Myelin Oligodendrocyte Glycoprotein (MOG) 35-55 alongside an adjuvant, mice show the same demyelination found in MS and exhibit similar symptoms. In both MS and the EAE model, CD4 T cells have been implicated as major contributors of autoimmune disease. However, both CD8 and CD4 T cells are present in MS lesions (Konjevic et al). In this study, we look specifically at a type of CD8 T cell present in the CNS of mice induced with EAE. This T cell, CD8aa, expresses an alpha homodimer instead of the classical alpha-beta heterodimer present in conventional CD8 T cells. Proposed to have an inhibitory function, these CD8aa cells are only significantly present in sick mice. We show that CD8aa expression correlates with disease severity, that these cells have a central memory phenotype, and that their expression of NK like markers acts to dampen the autoimmune response during EAE. Investigation into these cells could have major implications for future treatment of MS, allowing the targeting of effector CD8 T cells while leaving the CD8aa cells intact.