Project Description

Multiple sclerosis (MS) is an autoimmune disease in which immune cells attack neurons. When an immune response terminates, memory cells remain in the body in order to respond more effectively in future encounters. Previous studies found that the E12 antibody can increase differentiation of T-cells into T-type regulatory cells (Tr1), that secrete the cytokine IL-10 which represses abnormal immune responses. Our research examines whether E12 can increase their differentiation into memory cells. MS mice models treated with E12 showed substantial a reduction in clinical symptoms, and an increase in memory cells and IL-10 secretion compared to control. This indicates that Tr1 cells induced by E12 function as memory cells that can respond more effectively to the disease in future relapses.