The article aims to analyze pathogenetic mechanisms of autoimmune diseases development including disorders of both cellular and humoral immunity. The standard drug therapy with corticosteroids and cytostatics leads to a number of side effects such as lipid metabolism disorders (Kushing-syndrome), arterial hypertension, diabetes, and osteoporosis each of which is to be additionally treated. Chimeric monoclonal antibodies (rituximab, natalizumab, etc.) can also cause complications. Therefore apheresis therapy with removal of autoantibodies, circulating immune complexes and other pathological metabolites is pathogenetically justified. However, the greatest effect is reached by means of extracorporeal immunopharmacotherapy when, besides antibodies removal by means of plasmapheresis one performs selection of lymphocytes and their temporary incubation with very small doses of corticosteroids and cytostatics, which are then returned to the patient. The result is a significant reduction in levels of not only autoantibodies, but cytokines, which can be seen in the table. Cytokine levels during and after the course of extracorporeal immunopharmacotherapy (n=59) Stages TNF-α picogram/ml INF-γ picogram/ml IL-2 picogram/ml Before treatment 35.3±3.36 103.4±8.45 45.6±3.6 After treatment 28.2±2.21* 41.5±3.98* 40.3±3.6 In 6 months 29.85±2.32 77.48±5.4* 42.2±3.7 • Change from baseline statistically significant (p<0.05) Such targeted immunosuppression is much more effective then "pulse therapy" with minimum negative consequences for the body. At the same time a supporting drug therapy can be carried out with half smaller doses.
Key words: autoimmune diseases, cellular immunity, plasma exchange, extracorporeal immunopharmacotherapy, immunosuppression, fibrosing alveolitis, multiple sclerosis, rheumatoid arthritis, Crohn’s disease.