rspНаучно-практическая ревматологияRheumatology Science and Practice1995-44841995-4492IMA-PRESS, LLC10.14412/1995-4484-2015-299-307rsp-2093Research ArticleПРОГРЕСС В РЕВМАТОЛОГИИ В XXI ВЕКЕPROGRESS IN RHEUMATOLOGY IN THE XXI CENTURYСовременный взгляд на патогенез спондилоартритов – молекулярные механизмыMODERN IDEA ON THE PATHOGENESIS OF SPONDYLOARTHRITIS: MOLECULAR MECHANISMSНасоновЕ. Л.NasonovE. L.ГалушкоЕ. А.GalushkoE. A.

заведующая учебно-методическим отделом с центром информационных технологий ФГБНУ НИИР им. В.А. Насоновой, докт. мед. наук

orgcom@irramn.ruГордеевА. В.GordeevA. V.

профессор, ведущий научный сотрудник лаборатории микроциркуляцииФГБНУ НИИР им. В.А. Насоновой, докт. мед. наук

ФГБНУ Научно-исследовательский институт ревматологии им. В.А. Насоновой, Москва, Россия 115522 Москва, Каширское шоссе, 34АРоссияV.A. Nasonova Research Institute of Rheumatology, Moscow, Russia 34A, Kashirskoe Shosse, Moscow 115522Russian Federation201509092015533299307Copyright © Насонов Е.Л., Галушко Е.А., Гордеев А.В., 20152015Насонов Е.Л., Галушко Е.А., Гордеев А.В.Nasonov E.L., Galushko E.A., Gordeev A.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://rsp.mediar-press.net/rsp/article/view/2093

В настоящее время одним из основных звеньев патогенеза спондилоартритов (СпА) считается нарушение иммунного гомеостаза слизистой оболочки кишечника у генетически предрасположенных лиц, что приводит к развитию системного хронического воспаления. Результаты исследований последних лет позволяют говорить о ключевой роли оси интерлейкин 23/интерлейкин 17 (ИЛ23/ИЛ17) в развитии этих заболеваний. Многофакторные звенья патогенеза СпА характеризуются не только гиперпродукцией ИЛ23, но и изменением чувствительности к этому цитокину клеток-мишеней с параллельным увеличением их числа, что приводит к хроническому аутовоспалительному процессу, который реализуется через широкий спектр клинических проявлений различных вариантов СпА.

As of now, impaired immune homeostasis of the intestinal mucosa in genetically predisposed individuals is considered to be one of the major components in the pathogenesis of spondyloarthritis (SpA), which leads to systemic chronic inflammation. The results of recent studies may suggest that the interleukin-23/interleukin-17 (IL-23/IL-17) axis plays a leading role in the development of these diseases. The multifactorial components of the pathogenesis of SpA are characterized by not only the hyperproduction of IL-23, but also by the change in cell target susceptibility to this cytokine with aconcurrent increase in their number, resulting in the chronic autoinflammatory process that occurs via a wide spectrum of clinical manifestations of different types of SpA

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