Demyelinating disease: an immunological model for studies of neural antigens

Studies have shown that the parent myelin basic protein (MBP) is a more potent antigen than its disease-inducing fragments. Based on equimolar ratios, 10-15 times more peptide is required to induce experimental allergic encephalomyelitis (EAE) with the same severity as that induced by the intact MBP. In this report, we show that 2 epitopes are required for EAE in Lewis rats; that which induces T cell-mediated immunity requires the expression of a B cell epitope for the development of full spectrum of clinical and histopathological signs of disease. Thus, the development of disease may be related to the magnitude of the humoral and cellular responses to particular B and T cell epitopes. Whether more than 1 epitope, over 30 of which have been located in the MBP, contribute to the development of MBP-induced disease is not clear; but what is clear is that the EAE-inducing peptide sequence, unlike the MBP, is restricted in terms of the number of recognizable epitopes.