Новые возможности фармакотерапии иммуновоспалительных ревматических заболеваний: фокус на ингибиторы интерлейкина-17

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В последние годы большое внимание привлечено к Тh17-клеткам, синтезирующим интерлейкин 17 (ИЛ17), в отличие от Th1- и Тh2-клеток, «маркерными» цитокинами которых являются соответственно интерферон ү (ИФНү) и ИЛ4. Полагают, что именно патологическая активация и экспансия ТҺ17-клеток играют ведущую роль в развитии широкого спектра иммуновоспалительных заболеваний (ИВЗ) человека, включая ревматоидный артрит (РА), псориаз, анкилозирующий спондилит (АС), псориатический артрит (ПсА), воспалительные заболевания кишечника, системную красную волчанку, которые ранее рассматривались как Тh1-зависимые заболевания, связанные в первую очередь с гиперпродукцией ИЛ2 и ИФНү. Это послужило мощным стимулом для разработки новых генно-инженерных биологических препаратов, механизм действия которых основан на блокировании патологических эффектов ИЛ17, других связанных с активацией Тh17-клеток цитокинов, или «малых молекул», интерферирующих с факторами транскрипции, регулирующими синтез этих цитокинов. В обзоре обсуждаются современные исследования, касающиеся механизмов регуляции образования и функциональной активности цитокинов семейства ИЛ17, и доказательства значения этих цитоки-нов в патогенезе ИВЗ. Особое внимание уделяется клинической эффективности и безопасности моноклональных антител к ИЛ17А - препарату секукинумаб - при псориазе, ПсА, АС и РА.

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Ось ил17/ил23, интерлейкин 17, псориаз, псориатический артрит, анкилозирующий спондилит, ревматоидный артрит

Короткий адрес: https://sciup.org/14945797

IDR: 14945797   |   DOI: 10.14412/1995-4484-2017-68-86

Список литературы Новые возможности фармакотерапии иммуновоспалительных ревматических заболеваний: фокус на ингибиторы интерлейкина-17

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