Репозиторий Университета

© 2018 Ima-Press Publishing House. All rights reserved. Still's disease in children (systemic-onset juvenile idiopathic arthritis, SoJIA) and in adults (adult-onset Still's disease) are considered as non-familial systemic autoinflammatory diseases of unknown etiology driven by similar immunopathogenetic mechanisms. The adult-onset Still's disease pathogenesis is based on genetically determined innate immunity disturbances and molecular basis of immunopathogenesis consists of NLRP3 inflammasome-dependent mechanisms of inflammation characterized by hyperproduction of proinflammatory cytokines interleukin (IL) 1 and IL18. Nonsteroidal anti-inflammatory drugs, glucocorticoids, methotrexate and other disease modifying drugs are considered as «first line» medications for the treatment of adult-onset Still's disease and if they fail biologi-cals are recommended. A review of the literature data concerning anti-IL1 monoclonal antibodies administration in adult-onset Still's disease is presented, indicating good prospects for the use of canakinumab not only in case of resistance to standard therapy, but also as a «first-line» therapy in the onset of the disease.

© 2018 Ima-Press Publishing House. All rights reserved. Atherosclerosis is now considered as chronic inflammatory vascular disease connected to «pathological» activation of innate and adaptive immunity, characterized by lipid deposition, leukocyte infiltration and proliferation of vascular smooth muscle cells. Subclinical (low grade) inflammation plays fundamental role at all stages of atherosclerotic process progression and determines cardiovascular catastrophes development and mortality. Proinflammatory cytokines including interleukin (IL) 1, IL6, tumor necrosis factor α (TNFα), IL17, IL18, IL27, IL33, IL37 tightly interacting within cytokine network occupy an important place among numerous mediators participating in immunopathogenesis of atherosclerosis and rheumatoid arthritis. IL1β playing an important role in the development of many acute and chronic immunoinflammatory diseases attracts particular attention. IL1β significance in the development of atherosclerosis is determined by many mechanisms including procoagulant activity, enhancement of monocytes and leucocytes adhesion to vascular endothelium, vascular smooth muscle cells growth and others. Fundamental role of inflammation in the development of atherosclerosis is well proved in investigations of anti-atherosclerotic effect of canakinumab. Randomized placebo-controlled trial CANTOS (Canakinumab ANti-inflammatory Thrombosis Otcomes Study) assessing efficacy of canakinumab as new tool for secondary prophylaxis cardiovascular complications in general population of patients with severe atherosclerotic vascular damage. CANTOS results in combination with accumulated in rheumatology data on cardiovascular effects of anti-inflammatory drugs are of great importance for personification of approach to secondary prophylaxis of caused by atherosclerosis cardiovascular complications. They also contribute to the development of inflammatory theory of atherosclerosis pathogenesis in the whole.

© 2018 Ima-Press Publishing House. All rights reserved. Human immuno-inflammatory diseases (IID), depending on the predominant mechanisms of immune activation, are divided into two main categories: autoimmune and autoinflammatory. It is assumed that hyperproduction of "proin-flammatory" and immunoregulatory cytokine-interleukin 1 (IL 1) largely determines the "intersection" between the mechanisms underlying autoimmunity and autoinflammation in many IID. This review discusses the role of IL1 in the pathogenesis of IID, primarily those associated with the activation of NLRP3-inflammasome, and therapeutic perspectives of IL1β inhibition with monoclonal antibodies to IL1β - canakinumab. The study of the IL1 role in the regulation of interactions between innate (TLR activation, inflammasome) and adaptive (Th1 - and Th17-types of immune response) immunity and the efficacy of IL1 inhibitors may be important in terms of decoding the patho-genetic mechanisms of IID and the development of new approaches to personalized therapy.