Progress in the research of cellular and hunloral immumty has been exponential during the past decade, although it is still insufficient to explain fidly the pa~, bogenesis of autoimmunity. Over the same period, an understanding of the cytokine network and the extracelh: lar praterdysis cascades has grown considerably. Here, Ghisl, lin Opdenakker and Jo Van Damme propose the REGA-model (Remnant Epitope Generates Autoimmunity) to explain the generation of autoantigens and their interaction with the T-ceil receptor complex. Although this model may be applied to all known autoimmune diseases,, mdtip!-z sclerosis has been used as the specific example here.

Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system (CNS) and appears to be an immune disorder that is influenced by genetic and environmental factors. The specific immune response in MS and in experimental allergic encephalomyelitis (EAE) has recently been reviewedJ-L However, autoimmune diseases such as MS are also disorders of nonspecific immunity. In this article, a model is presented to explain the importance of nonspecificity. The model incorporates informatio~ derived from clinical and experimental research and proposes novel roles for cells of the immune system in autoimmune diseases.