Unfortunately, there are a variety of mechanisms including molecular mimicry, bystander activation, exposure of cryptic antigens, and superantigens by which pathogens can aid in the expression of an autoimmune disease [16] [17] [18] [19] [20] [21] . Inflammation induced by exposure to a foreign antigen can lead to autoimmune diseases from cross-reactive epitopes (molecular mimicry). These epitopes are segments of foreign antigens which, when presented to either T or B cells in the context of the MHC, can activate CD4 + or CD8 + T cells. The induction of the immune response and subsequent proinflammatory cytokine release is critical for clearance of a virus or bacteria. However, a sustained proinflammatory response against specific host tissues can occur when there is sequence or structural homology between foreign antigens and selfantigens, termed molecular mimicry [18] . Although this concept has been associated with autoimmunity, there are instances where mimicry (cross-reactivity) provides protection for the host, termed heterologous immunity [22] . Cross-reactivity or mimicry between various strains of viruses or bacteria could help explain how protective immunity arises in certain individuals even in the absence of prior exposure to an emerging pathogen. This example of sequence homology in which molecular mimicry between viruses leads to protective immunity is in contrast to a pathogen mimicking host epitopes (reviewed in [11] ).