Using two mouse strains that spontaneously develop autoimmunity, namely the lupus-prone MRL/lpr strain and the non-obese diabetic (NOD) mouse, and the myelin oligodendrocyte glycoprotein (MOG)-induced mouse model for multiple sclerosis [experimental autoimmune encephalomyelitis (EAE)], we provide evidence that prenatal betamethasone treatment, by inducing changes in the T cell repertoire, can alter the course of autoimmune disease. This evidence concerns the gene MOG and multiple sclerosis.