What is it about?
Molecular mimicry is well-established as a trigger for different autoimmune diseases but is usually restricted to exploring clinically relevant pathogens. We start from a different perspective that any human-associated microorganism (pathogen or commensal) could trigger an autoimmune process if harbouring the capacity to mimic disease-related autoantigens, which we systematically explore (through custom immunoinformatics protocol) on the example of T-cell epitopes related to Rheumatoid Arthritis, as one of the most incident autoimmune diseases worldwide. In this sense, we discovered a number of, previously unrecognized, human pathogens and commensals as potential triggers of Rheumatoid Arthritis and highlighted for the first time the high potential of fungal pathogens ad commensals to elicit RA-directed autoimmunity.
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Why is it important?
Studies of this kind help identify additional environmental risk factors for the etiology of Rheumatoid Arthritis, opening an avenue for prophylaxis in genetically predisposed individuals in terms of microbiota-based therapeutics. Besides prophylaxis, identification of most likely mimicked autoantigens/epitopes is a first step towards designing next-generation, autoantigen-based therapeutics, in search for durable, medication-free disease remission.
Perspectives
In addition to investigating mechanisms behind autoimmunity, analysis of microbial-derived mimotopes is also important for the development of novel, autoantigen-based therapies, since the screening of the most immunogenic epitope/mimotopes can direct the design of multivalent peptide vaccines for Rheumatoid Arthritis. The main aim of such therapeutics would be to restore to identified, most potent autoantigens, rather than inducing general suppression of immune system functioning.
Bojan Božić
University of Belgrade, Faculty of Biology, Institute of Physiology and Biochemistry “Ivan Djaja”, Belgrade, Serbia
Read the Original
This page is a summary of: Mining the capacity of human-associated microorganisms to trigger rheumatoid arthritis—A systematic immunoinformatics analysis of T cell epitopes, PLOS One, June 2021, PLOS,
DOI: 10.1371/journal.pone.0253918.
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