The role of interleukin 1 in the development of human diseases
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...
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doaj-e09479294c304881829a0dc48cda98632021-08-02T09:05:52ZrusIMA-PRESS LLCНаучно-практическая ревматология1995-44841995-44922019-04-01560192710.14412/1995-4484-2018-19-272461The role of interleukin 1 in the development of human diseasesE. L. Nasonov0V.A. Nasonova Research Institute of Rheumatology; I.M. Sechenov First Moscow State Medical University (Sechenov University), Ministry of Health of RussiaHuman 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.https://rsp.mediar-press.net/rsp/article/view/2686immunoinflammatory diseasesinterleukin 1inflammasomecanakinumab |
collection |
DOAJ |
language |
Russian |
format |
Article |
sources |
DOAJ |
author |
E. L. Nasonov |
spellingShingle |
E. L. Nasonov The role of interleukin 1 in the development of human diseases Научно-практическая ревматология immunoinflammatory diseases interleukin 1 inflammasome canakinumab |
author_facet |
E. L. Nasonov |
author_sort |
E. L. Nasonov |
title |
The role of interleukin 1 in the development of human diseases |
title_short |
The role of interleukin 1 in the development of human diseases |
title_full |
The role of interleukin 1 in the development of human diseases |
title_fullStr |
The role of interleukin 1 in the development of human diseases |
title_full_unstemmed |
The role of interleukin 1 in the development of human diseases |
title_sort |
role of interleukin 1 in the development of human diseases |
publisher |
IMA-PRESS LLC |
series |
Научно-практическая ревматология |
issn |
1995-4484 1995-4492 |
publishDate |
2019-04-01 |
description |
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. |
topic |
immunoinflammatory diseases interleukin 1 inflammasome canakinumab |
url |
https://rsp.mediar-press.net/rsp/article/view/2686 |
work_keys_str_mv |
AT elnasonov theroleofinterleukin1inthedevelopmentofhumandiseases AT elnasonov roleofinterleukin1inthedevelopmentofhumandiseases |
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1721235696900898816 |