БИОХИМИЯ, 2021, том 86, вып. 11, с. 1654–1667

УДК 577.571.27

Роль транскрипционного фактора STAT3 в патогенезе бронхиальной астмы

Обзор

© 2021 А.А. Никольский, И.П. Шиловский *ip.shilovsky@nrcii.ru, Е.Д. Барвинская, А.В. Корнеев, М.С. Сундукова, М.Р. Хаитов

ФГБУ «ГНЦ Институт иммунологии» ФМБА России, 115522 Москва, Россия

Поступила в редакцию 01.04.2021
После доработки 21.09.2021
Принята к публикации 12.10.2021

DOI: 10.31857/S032097252111004X

КЛЮЧЕВЫЕ СЛОВА: бронхиальная астма, STAT3, JAK, Т-хелперы, сигнальный путь.

Аннотация

Бронхиальная астма – это гетерогенное хроническое воспалительное заболевание дыхательных путей. Исследования молекулярных и клеточных механизмов бронхиальной астмы позволили установить, что в её патогенез вовлечён широкий спектр клеток иммунной системы (Т- и В‑клетки, эозинофилы, нейтрофилы, макрофаги и пр.), а также структурных клеток (эпителиальные и эндотелиальные). Эти клетки активируются в ответ на внешние стимулы (бактерии, вирусы, аллергены и прочие поллютанты) и продуцируют провоспалительные факторы (цитокины, хемокины, металлопротеиназы и пр.), что в итоге приводит к запуску патологических процессов в лёгких. Известно, что в активацию клеток вовлечены гены, кодирующие транскрипционные факторы семейства STAT (STAT – signal transducer and activator of transcription), которое насчитывает 7 представителей. Недавние исследования показали, что фактор транскрипции STAT3 играет важную роль в активации вышеуказанных клеток и тем самым вносит вклад в развитие астмы. В исследованиях на животных селективное ингибирование STAT3 значительно уменьшает выраженность воспаления в лёгких, что свидетельствует о его перспективности как терапевтической мишени. В данном обзоре мы описываем механизмы активации STAT3 и его роль в поляризации Th2/Th17-клеток и М2‑макрофагов в дисфункции эндотелиальных клеток, что в итоге приводит к формированию проявлений бронхиальной астмы: инфильтрации лёгких эозинофилами и нейтрофилами, гиперреактивности бронхов и ремоделированию респираторного тракта.

Сноски

* Адресат для корреспонденции.

Финансирование

Исследование выполнено при финансовой поддержке Российского фонда фундаментальных исследований (грант № 20‑34‑90151).

Конфликт интересов

Авторы заявляют об отсутствии конфликта интересов.

Соблюдение этических норм

Настоящая статья не содержит описания каких-либо исследований с участием людей или животных в качестве объектов.

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