Autoimmune disease has long been considered a shadow following infectious diseases. Epidemiological evidence shows that infectious disease follows streptococcal infection andTrypanosoma cruziinfection is that the instigator of Chagas’ disease. There is, however, little or no information of the mechanism by which such a train of events is initiated. Autoimmunity, during a sort of autoantibodies, is common after many infections and should well result from the mimicking of host proteins by antigens of the infective agent . There are, however, few if any examples in humans where molecular mimicry gives rise to autoimmune disorder . The progression from benign autoimmunity to pathogenic autoimmune disorder depends upon the balance of cytokines produced during the inflammatory process accompanying infection. In many autoimmune diseases, the cytokine profile favors the proinflammatory cytokines, IFN-γ and IL-1, which support the assembly of disease.