Editorial
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World J Dermatol. Nov 2, 2013; 2(4): 36-43
Published online Nov 2, 2013. doi: 10.5314/wjd.v2.i4.36
Molecular mimicry in cutaneous autoimmune diseases
Fabrizio Guarneri, Claudio Guarneri
Fabrizio Guarneri, Claudio Guarneri, Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy
Author contributions: Guarneri F designed the editorial and wrote the manuscript; Guarneri C reviewed the manuscript.
Correspondence to: Fabrizio Guarneri, MD, Professor, Department of Clinical and Experimental Medicine, University of Messina, AOU Policlinico “G. Martino”, Via Consolare Valeria 1, 98125 Messina, Italy. f.guarneri@tiscali.it
Telephone: +39-90-357070 Fax: +39-90-2927691
Received: August 12, 2013
Revised: September 2, 2013
Accepted: September 14, 2013
Published online: November 2, 2013
Core Tip

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.