MedElevator Войти в исследования
← Поиск публикаций

DOI 10.3390/ijms22063090

Медицинская библиотека · International journal of molecular sciences · 2021

Role of the Innate Immunity Signaling Pathway in the Pathogenesis of Sjögren's Syndrome.

Shimizu Toshimasa, Nakamura Hideki, Kawakami Atsushi

СтатьяОбзорПеревод в очереди

Аннотация

Sjögren's syndrome (SS) is a systemic autoimmune disease characterized by chronic inflammation of the salivary and lacrimal glands and extra-glandular lesions. Adaptive immune response including T- and B-cell activation contributes to the development of SS. However, its pathogenesis has not yet been elucidated. In addition, several patients with SS present with the type I interferon (IFN) signature, which is the upregulation of the IFN-stimulated genes induced by type I IFN. Thus, innate immune responses including type I IFN activity are associated with SS pathogenesis. Recent studies have revealed the presence of activation pattern recognition receptors (PRRs) including Toll-like receptors, RNA sensor retinoic acid-inducible gene I and melanoma differentiation-associated gene 5, and inflammasomes in infiltrating and epithelial cells of the salivary glands among patients with SS. In addition, the activation of PRRs via the downstream pathway such as the type I IFN signature and nuclear factor kappa B can directly cause organ inflammation, and it is correlated with the activation of adaptive immune responses. Therefore, this study assessed the role of the innate immune signal pathway in the development of inflammation and immune abnormalities in SS.

Для цитирования: Shimizu Toshimasa, Nakamura Hideki, Kawakami Atsushi. Role of the Innate Immunity Signaling Pathway in the Pathogenesis of Sjögren's Syndrome.. International journal of molecular sciences. 2021. DOI: 10.3390/ijms22063090.

Предметные рубрики MeSH

Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

История · было → стало

Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.

Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.