Translational pediatrics · 2026
FOS regulation of T-cell activation and the mechanism of inflammatory injury of coronary endothelium in Kawasaki disease.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
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.
Wang Shuhui, Tang Xuan, Ma Jin, Wang Nana, Wang Yan, Gao Yang, Huang Hongbiao, Qian Guanghui, Zhang Jiaying, Lv Haitao, Li Xuan
Аннотация
BACKGROUND: Kawasaki disease (KD) is a pediatric systemic vasculitis often causing coronary lesions driven by aberrant T-cell activation. While FOS modulates T cells, its specific function in KD remains undefined. This study aims to investigate the role of FOS in T-cell activation and coronary endothelial inflammation in KD.
METHODS: The study integrated transcriptomic profiling of T cells from patients with KD and a murine model of Candida albicans water-soluble fraction (CAWS)-induced vasculitis to characterize FOS expression and vasculitis. Mechanistically, we employed lentiviral modulation of FOS in activated JURKAT cells co-cultured with human coronary artery endothelial cells (HCAECs) to delineate the impact of FOS on T-cell activation and endothelial inflammation.
RESULTS: Compared to controls, FOS expression was significantly upregulated in peripheral blood T cells of acute KD patients (P<0.001). FOS levels were also elevated in peripheral blood T cells and cardiac inflammatory regions of the KD model mice, and inhibition of FOS expression attenuated vasculitis. CD3/28 magnetic bead stimulation increased FOS expression in JURKAT cells, along with elevated levels of inflammatory cytokines interleukin-6 and tumor necrosis factor. Co-culture of activated JURKAT cells with HCAECs resulted in marked endothelial inflammation. Conversely, knocking down FOS in JURKAT cells prior to activation and co-culture mitigated endothelial inflammation.
CONCLUSIONS: FOS contributes to the development and progression of coronary endothelial inflammation in KD by modulating T-cell activation. Targeting FOS may represent a potential therapeutic strategy for mitigating KD-associated coronary artery injury.
METHODS: The study integrated transcriptomic profiling of T cells from patients with KD and a murine model of Candida albicans water-soluble fraction (CAWS)-induced vasculitis to characterize FOS expression and vasculitis. Mechanistically, we employed lentiviral modulation of FOS in activated JURKAT cells co-cultured with human coronary artery endothelial cells (HCAECs) to delineate the impact of FOS on T-cell activation and endothelial inflammation.
RESULTS: Compared to controls, FOS expression was significantly upregulated in peripheral blood T cells of acute KD patients (P<0.001). FOS levels were also elevated in peripheral blood T cells and cardiac inflammatory regions of the KD model mice, and inhibition of FOS expression attenuated vasculitis. CD3/28 magnetic bead stimulation increased FOS expression in JURKAT cells, along with elevated levels of inflammatory cytokines interleukin-6 and tumor necrosis factor. Co-culture of activated JURKAT cells with HCAECs resulted in marked endothelial inflammation. Conversely, knocking down FOS in JURKAT cells prior to activation and co-culture mitigated endothelial inflammation.
CONCLUSIONS: FOS contributes to the development and progression of coronary endothelial inflammation in KD by modulating T-cell activation. Targeting FOS may represent a potential therapeutic strategy for mitigating KD-associated coronary artery injury.