Prospects for the study of transposons in the pathogenesis of autoimmune diseases

One of the mechanisms for development autoimmune diseases is changes in epigenetic regulation, root causes which have not yet been established. At same time, data on role transposons as sources long noncoding ribonucleic acids (RNA) and microRNAs involved immune pathology accumulated. In evolution, transposable elements become basis emergence V(D)J recombination regulation HLA genes. Pathological transposon activation has revealed type 1 diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus, AicardiGoutieres Sjgrens syndromes. The influence exogenous viruses may be due to their interactions with transposons. Transposable themselves are able activate antiviral response, stimulating hyperproduction interferon. An assumption about drivers was made, reflected expression non-coding RNAs, key factors. analysis transposon-derived microRNA database (MDTE DB) made it possible identify 13 associated diseases: scleroderma (miR-31, miR-609, miR-3162), juvenile arthritis (miR-151), erythematosus (miR-198, miR-342), psoriasis (miR-224, miR-378) myasthenia gravis (miR-421, miR-551a, miR-612, miR-891b), multiple sclerosis (miR-584 ), serves a proof proposed hypothesis. Since factors under reversible certain targeted therapy using analogues tools promising direction specific treatment diseases.