Revised: September 2, 2013
Accepted: September 14, 2013
Published online: November 2, 2013
The emulation of characteristics of a different organism to gain biological advantage is a common phenomenon in nature, described and defined with the term “mimicry” in the second half of the 19th century. In the last decades, mimicry at molecular level has been evidenced as a method used by several pathogen microrganisms to control metabolic functions of infected cells and elude host’s immune system. Because of molecular mimicry, immune reactions against microbial molecules can turn against the mimicked self-molecules in predisposed subjects, leading to autoimmunity. This pathogenic mechanism, which gives a possible explanation for the specific epidemiological and chronological association between some infections and some autoimmune diseases, is well known and verified in many fields of medicine, but not adequately studied in dermatology: experimental data are available only for leprosy, atopic dermatitis, Behçet’s disease, Vogt-Koyanagi-Harada syndrome and systemic erythematous lupus, while for few other diseases its role is hypothetical or suggested on the basis of single, small experiments or anecdotal reports. An overview of available data and hypotheses about the role of molecular mimicry in autoimmune cutaneous diseases is presented here, together with the perspectives offered by the use of bioinformatics and the personal experience of the author in this field.
Core tip: Molecular mimicry between microbial and human proteins is often used by pathogens to control biosynthetic/regulatory pathways of infected cells and elude immune reaction of host. In predisposed subjects, immune response against non-self molecules can, because of molecular mimicry, turn against self antigens and trigger autoimmune diseases. This mechanism, which explains the specific epidemiological link between some infections and some autoimmune diseases, is known and experimentally confirmed in several disciplines, but much less studied in dermatology. Bioinformatics can greatly help and boost research by quickly and almost inexpensively identifying molecules most probably involved in triggering autoimmunity via molecular mimicry.