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Dimethyl fumarate alleviates allergic asthma by strengthening the Nrf2 signaling pathway in regulatory T cells.
Cen, Yanhong; Li, Fangfang; Li, Yikui; Zhang, Kaimin; Riaz, Farooq; Zhao, Kuaile; Wei, Ping; Pan, Fan.
Afiliación
  • Cen Y; Department of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
  • Li F; Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
  • Li Y; Department of Otolaryngology, West China Second University Hospital, Sichuan University, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu, China.
  • Zhang K; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
  • Riaz F; Shanghai Clinical Research Center for Radiation Oncology, Shanghai, China.
  • Zhao K; Shanghai Key Laboratory of Radiation Oncology, Shanghai, China.
  • Wei P; Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
  • Pan F; Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Front Immunol ; 15: 1375340, 2024.
Article en En | MEDLINE | ID: mdl-38711519
ABSTRACT
Allergic asthma is a widely prevalent inflammatory condition affecting people across the globe. T cells and their secretory cytokines are central to the pathogenesis of allergic asthma. Here, we have evaluated the anti-inflammatory impact of dimethyl fumarate (DMF) in allergic asthma with more focus on determining its effect on T cell responses in allergic asthma. By utilizing the ovalbumin (OVA)-induced allergic asthma model, we observed that DMF administration reduced the allergic asthma symptoms and IgE levels in the OVA-induced mice model. Histopathological analysis showed that DMF treatment in an OVA-induced animal model eased the inflammation in the nasal and bronchial tissues, with a particular decrease in the infiltration of immune cells. Additionally, RT-qPCR analysis exhibited that treatment of DMF in an OVA-induced model reduced the expression of inflammatory cytokine (IL4, IL13, and IL17) while augmenting anti-inflammatory IL10 and Foxp3 (forkhead box protein 3). Mechanistically, we found that DMF increased the expression of Foxp3 by exacerbating the expression of nuclear factor E2-related factor 2 (Nrf2), and the in-vitro activation of Foxp3+ Tregs leads to an escalated expression of Nrf2. Notably, CD4-specific Nrf2 deletion intensified the allergic asthma symptoms and reduced the in-vitro iTreg differentiation. Meanwhile, DMF failed to exert protective effects on OVA-induced allergic asthma in CD4-specific Nrf2 knock-out mice. Overall, our study illustrates that DMF enhances Nrf2 signaling in T cells to assist the differentiation of Tregs, which could improve the anti-inflammatory immune response in allergic asthma.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Asma / Transducción de Señal / Linfocitos T Reguladores / Factor 2 Relacionado con NF-E2 / Dimetilfumarato Límite: Animals Idioma: En Revista: Front Immunol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Asma / Transducción de Señal / Linfocitos T Reguladores / Factor 2 Relacionado con NF-E2 / Dimetilfumarato Límite: Animals Idioma: En Revista: Front Immunol Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza