Abstract
Autoimmune diseases emerge due to several reasons, of which molecular mimicry i.e., similarity between the host's and pathogen's interacting peptides is an important reason. In the present study we have reported a database of only experimentally verified peptide sequences, which exhibit molecular mimicry. The database is named as miPepBase (Mimicry Peptide Database) and contains comprehensive information about mimicry proteins and peptides of both host (and model organism) and pathogen. It also provides information about physicochemical properties of protein and mimicry peptides, which might be helpful in predicting the nature of protein and optimization of protein expression. The miPepBase can be searched using a keyword or, by autoimmune disease(s) or by a combination of host and pathogen taxonomic group or their name. To facilitate the search of proteins and/or epitope in miPepBase, which is similar to the user's interest, BLAST search tool is also incorporated. miPepBase is an open access database and available at http://proteininformatics.org/mkumar/mipepbase.
Highlights
Mimicry is a very common phenomenon in which a living being pretends to be what it is not
With the passage of time, number of autoimmune diseases caused due to molecular mimicry is increasing
A unified repository of the available information related to molecular mimicry based autoimmune diseases is not available, we have built a database which contains the information regarding proteins and peptides associated with the process, but several other important details
Summary
Mimicry is a very common phenomenon in which a living being pretends to be what it is not. It is not surprising that similar strategy has been exploited at the molecular level as well. The obvious benefit molecular mimicry confers to pathogens is to fool the host’s defenses and survive. The presence of a molecule in a pathogen that is similar with a host antigen could inhibit the immune response of the host against the pathogen because of the immune tolerance toward self-antigens (Davies, 1997; Gowthaman and Eswarakumar, 2013). Helicobacter pylori infection in human triggers two autoimmune diseases namely autoimmune gastritis and pernicious anemia. It occurs because activated CD4+ Th1 cells infiltrates into gastric mucosa and they cross-recognize the self-epitopes of H+K+ ATPase and H. pylori antigens (D’Elios et al, 2004)
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