Another hypothesis is the concept of molecular mimicry based on the similarity of pathogen and host antigenderived epitopes recognized by the immune system [162, 163] , which render bacteria and viruses candidates for the induction of autoimmune disease. This mechanism has first been suggested to be responsible for the development of rheumatic fever, and though this could never be confirmed, there is evidence suggesting associations of infectious triggers for several systemic autoimmune diseases including multiple sclerosis [164, 165] , systemic lupus erythematosus (SLE) [166] , and rheumatoid arthritis [167] . Autoantigens are unable to elicit a primary immune response themselves. However, T cells stimulated by a pathogenic cross-reactive epitope can recognize such targets. As a prerequisite, the pathogen-derived cross-reactive epitope has to be sufficiently different from the host-derived epitope. The role of infectious agents in development of autoimmunity has recently been reviewed elsewhere [168, 169] .