Synopsis of Paper Entitled “Ir Gene Expression, Antigen Processing and Autoantigen Characterization in Autoimmune Diseases of the Nervous System”

Abstract

Dr Wekerle began by highlighting the problems associated with the investigation of patients with multiple sclerosis. Whilst he thought it very likely that the disease was an autoimmune one, he reminded the audience that we still do not know what the target autoantigen is, have almost no access to the target tissue and, are as yet, unable to transfer the disease with human material. He suggested therefore that most of our knowledge on multiple sclerosis, to date, had to rely on animal models of the disease. He went on to highlight the two animal models that he had worked with; the first is the EAE Lewis rat in which the disease is inducible with myelin or myelin basic protein (MBP) in complete Freund’s adjuvant. He pointed out that the T cells and the pathogenesis of this disease were CD4+ T cells which were specific for MBP. In the mouse models that he has worked with, he reported that differences in haplotypes in mice lead to differences in the epitopes of the MBP autoantigen that they recognize so that, for example, the PL/J mice see the 1–11 amino acid sequence of the autoantigen, whereas the SJL/J mice see the 90–101 amino acid sequence. In contrast, the Lewis rat encephalytogenic T cell clones seemed to be seeing the amino acid sequence 68–88 of MBP. Using these T cell clones it was possible to show that they transferred disease.