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Significant progress related particular to the use of interleukin (IL)-6 and IL17 inhibitors has been made in the pharmacotherapy of rheumatic diseases. IL-6 is a cytokine that has a wide range of biological activity and affects different types of cells. There is evidence for the important role of IL-6 hyperproduction not only in rheumatoid arthritis (RA), but also in other immune inflammatory rheumatic diseases (systemic lupus erythematosus (SLE), scleroderma system atica, idiopathic inflammatory myopathies, giant cell arteritis, etc.). IL-6 inhibition primarily with humanized monoclonal antibodies against IL-6 receptors (tocilizumab – TCZ)) is considered as one of the promising areas of pharmacotherapy for these diseases. The successful results of TCZ use have created pre requisites for the design of other medicaments that can form a novel class of IL-6 inhibitors, genetically engineered biological agents, in the future. There is another new area in the treatment of immune inflammatory rheumatic diseases, which is the inhibition of the cytokine IL17A that provides interaction between innate and acquired immunity and is synthesized by a wide range of immunocompetent cells, the socalled Th17 ones in particular. IL-17A is implicated in the immunopathogenesis of a broad spectrum of immune inflammatory diseases, including RA, psoriasis, psoriatic arthritis, inflammatory bowel diseases, SLE, allergic diseases, transplantation immunity, obesity, carcinogenesis, etc. Elevated IL-17A concentrations correlate with the activity and severity of a pathological process. The pathogenetic effects of IL-17 in RA may be associated with its involvement in the development of synovial inflammation and joint destruction. The therapeutic efficiency of inhibition of Th17 cells and IL-17A synthesis in autoimmune diseases was first indirectly demonstrated in psoriasis. This provided the basis for the elaboration of therapeutic approaches associated with the direct inhibition of IL-17 effects in these patients. Thus, the use of IL-6 inhibitors (primarily TCZ) and, probably, IL-17 will make significant progress in the treatment of not only RA, but other severe potentially deadly immune inflammatory rheumatic diseases in the future.

The paper analyzes the efficiency and tolerability of a combination of rituximab (RTM) and leflunomide (LEF) for the treatment of rheumatoid arthritis (RA) versus the conventional combination of RTM and methotrexate (MT). The results of 24-week therapy were assessed in the RA patients included into the Russian Biological Therapy Register. A good effect of therapy was achieved in 31.8% of the patients who had received RTM+LEF (p = 0.1). The development of clinical remissions in RA was observed at a practically equal frequency of 13.6 and 11.7%, respectively. The doses of glucocorticoids and nonsteroidal anti-inflammatory drugs used in concurrent anti-inflammatory therapy could be substantially reduced in both groups. In both groups, the rate of side effects was very equal: 21.7% for the RTM+LEF group and 25.7% for the RTM+MT group. Thus, the combination therapy of RTM and LEF in real clinical practice is not considerably different from the most commonly used combination of RMT and MT in efficiency and tolerability and may be successfully used if there are any contraindications to the use of MT.

As of now, there have been notable advances in treating immune inflammatory rheumatic diseases, which are associated with the interpretation of basic pathogenetic mechanisms of their development. The most well studied therapeutic targets are tumor necrosis factor-α, interleukin (IL)-6 and IL-1; inhibition of these cytokines with genetically engineered biological agents is not always clinically effective and rarely gives rise to remission. The new promising treatment of rheumatoid arthritis (RA) and other inflammatory arthritides is linked to the inhibition of IL-17A, a proinflammatory cytokine, involved in the development of inflammation and in the destruction of bone tissue. The paper summarizes new evidence for the prospects of using anti-interleukin-17 monoclonal antibodies to treat RA.