Репозиторий Университета

© 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.