Disease mimicry—a pathogenetic concept for T cell-mediated autoimmune disorders triggered by molecular mimicry?

Molecular mimicry is considered as a mechanism by which infectious pathogens may break immunological tolerance and cause autoimmune disease. It implicates that peptides shared between pathogen and host may induce cross-reactive immune reactions. According to this hypothesis, the resulting autoimmune response actually represents a secondary immune response. It is mediated by cross-reactive T cells that have been educated in a primary immune response against a particular pathogen. Using psoriasis vulgaris as a model, this article discusses the potential functional consequences molecular mimicry should have for the resulting autoimmune disease. It proposes that due to the functional memory of T cells, which is an integral feature of adaptive immunity, the phenotype of an autoimmune disease induced by molecular mimicry should reflect the immune mechanisms raised in the primary immune response. This process might be called ‘disease mimicry’.