In the rheumatic diseases, there is a subgroup of illnesses which are sometimes called systemic rheumatic diseases and includes systemic lupus erythematosus, scleroderma, Sjogren's syndrome, mixed connective tissue disease, dermatomyositis and polymyositis, rheumatoid arthritis and drug-induced lupus. This subgroup is characterized by the presence of autoantibodies to nuclear and cytoplasmic autoantigens. Each of the diseases described above has a different profile of autoantibodies and there is now much evidence to show that the autoantibody response is antigen-driven. Molecular characterization of the structure and function of antigens has proceeded at a rapid pace, due to contributions from Immunologists and Molecular and Cell Biologists. However, the crucial question of why and how intracellular molecules become immunogenic has not been elucidated. One hypothesis is that autoantigens are rendered immunogenic because of mutations, alterations in structure and function, altered expression, or ectopic distribution - all of which are related to altered antigen as the driving principle behind the autoantibody response. Since 1989, there have been a series of Workshops on the Molecular and Cell Biology of Autoantibodies and Autoimmunity which started at the University of Heidelberg in Germany and has been held every two years in different institutions throughout the world. These workshops have encouraged closer contacts between Immunologists on the one hand and Molecular and Cell Biologists on the other and have been successful in promoting collaboration between these two groups of scientists.
The aim i s to facilitate greater interaction between these scientists and immunologists by face-to-face scientific exchanges and to address the clinically important question of the immunogenicity of autoantigens.
