rspНаучно-практическая ревматологияRheumatology Science and Practice1995-44841995-4492IMA-PRESS, LLC10.14412/1995-4484-2018-19-27rsp-2686Research ArticleОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯORIGINAL RESEARCHРоль интерлейкина 1 в развитии заболеваний человекаThe role of interleukin 1 in the development of human diseasesНасоновЕ. Л.NasonovE. L.

115522 Москва, Каширское шоссе, 34А;

кафедра ревматологии Института профессионального образования, 119991 Москва, ул. Трубецкая, 8, стр. 2

Department of Rheumatology, Institute of Professional Education, 34A, Kashirskoe Shosse, Moscow 115522;

8, Trubetskaya St., Build. 2, Moscow 119991

ФГБНУ «Научно-исследовательский институт ревматологии им. В.А. Насоновой», ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет)РоссияV.A. Nasonova Research Institute of Rheumatology; I.M. Sechenov First Moscow State Medical University (Sechenov University), Ministry of Health of RussiaRussian Federation201803042019560приложение 41927Copyright © Насонов Е.Л., 20192019Насонов Е.Л.Nasonov E.L.This work is licensed under a Creative Commons Attribution 4.0 License.https://rsp.mediar-press.net/rsp/article/view/2686

Иммуновоспалительные заболевания (ИВЗ) человека в зависимости от преобладающих механизмов активации иммунитета разделяются на две основные категории: аутоиммунные и аутовоспалительные. Предполагается, что гиперпродукция «провоспалительного» и иммунорегуляторного цитокина – интерлейкина 1 (ИЛ1) – во многом определяет «перекрест» между механизмами, лежащими в основе аутоиммунитета и аутовоспаления, при многих ИВЗ. В обзоре рассматриваются роль ИЛ1 в патогенезе ИВЗ, в первую очередь связанных с активацией NLRP3-инфламмасомы, и терапевтические перспективы ингибиции ИЛ1β с использованием моноклональных антител к ИЛ1β – канакинумаба. Изучение роли ИЛ1 в регуляции взаимодействия между врожденным (активация TLR, инфламмасомы) и приобретенным (Th1- и Th17-типы иммунного ответа) иммунитетом и эффективности ингибиторов ИЛ1 может иметь важное значение в плане расшифровки патогенетических механизмов ИВЗ и разработки новых подходов к персонифицированной терапии.

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 "proinflammatory" 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 pathogenetic mechanisms of IID and the development of new approaches to personalized therapy.

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The authors declare that there are no conflicts of interest present.