IFN-Gamma-mediated Regulation of Progression of Experimental Autoimmune Encephalomyelitis

Multiple sclerosis (MS) is the most common autoimmune disease of the central nervous system. It is a T cell mediated disease of unknown origin. The most common form of multiple sclerosis is the relapsing-remitting form (RRMS) and affects around 85% of individuals at initial diagnosis. This form of disease is characterized by episodes of increased disease severity(relapses) followed by periods of little to no disease (remission). Of the 85% originally diagnosed with RRMS, approximately 60% will progress to another form of MS, secondary progressive MS (SPMS) after 19 years of diagnosis. During SPMS, patients no longer fully remit after relapse. Importantly, the cause of progression of this disease is poorly understood. Therefore, investigating the involvement of critical inflammatory mediators such as IFN-γ in the progression of MS or it’s animal model experimental autoimmune encephalomyelitis (EAE), as well as developing a better understanding of the metabolic functions of immune cells and CNS cells, such as microglia and neurons, during neuroinflammation and unraveling the biology of memory T cells and B cells allows for novel insights into the mechanisms that drive progression of MS. The purpose of this study was therefore to elucidate mechanisms contributing to the progression of MS with a focus on metabolism, memory T cells, B cells, and IFN-γ.