دورية أكاديمية

Growth Arrest-Specific 6 Enhances the Suppressive Function of CD4+CD25+ Regulatory T Cells Mainly through Axl Receptor

التفاصيل البيبلوغرافية
العنوان: Growth Arrest-Specific 6 Enhances the Suppressive Function of CD4+CD25+ Regulatory T Cells Mainly through Axl Receptor
المؤلفون: Guang-ju Zhao, Jia-yi Zheng, Jia-lan Bian, Long-wang Chen, Ning Dong, Yan Yu, Guang-liang Hong, Arvine Chandoo, Yong-Ming Yao, Zhong-qiu Lu
المصدر: Mediators of Inflammation, Vol 2017 (2017)
بيانات النشر: Wiley, 2017.
سنة النشر: 2017
المجموعة: LCC:Pathology
مصطلحات موضوعية: Pathology, RB1-214
الوصف: Background. Growth arrest-specific (Gas) 6 is one of the endogenous ligands of TAM receptors (Tyro3, Axl, and Mertk), and its role as an immune modulator has been recently emphasized. Naturally occurring CD4+CD25+ regulatory T cells (Tregs) are essential for the active suppression of autoimmunity. The present study was designed to investigate whether Tregs express TAM receptors and the potential role of Gas6-TAM signal in regulating the suppressive function of Tregs. Methods. The protein and mRNA levels of TAM receptors were determined by using Western blot, immunofluorescence, flow cytometry, and RT-PCR. Then, TAM receptors were silenced using targeted siRNA or blocked with specific antibody. The suppressive function of Tregs was assessed by using a CFSE-based T cell proliferation assay. Flow cytometry was used to determine the expression of Foxp3 and CTLA4 whereas cytokines secretion levels were measured by ELISA assay. Results. Tregs express both Axl and Mertk receptors. Gas6 increases the suppressive function of Tregs in vitro and in mice. Both Foxp3 and CTLA-4 expression on Tregs are enhanced after Gas6 stimulation. Gas6 enhances the suppressive activity of Tregs mainly through Axl receptor. Conclusion. Gas6 has a direct effect on the functions of CD4+CD25+Tregs mainly through its interaction with Axl receptor.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 0962-9351
1466-1861
Relation: https://doaj.org/toc/0962-9351; https://doaj.org/toc/1466-1861
DOI: 10.1155/2017/6848430
URL الوصول: https://doaj.org/article/20ac27002ad0474982302e2599ab9f32
رقم الأكسشن: edsdoj.20ac27002ad0474982302e2599ab9f32
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:09629351
14661861
DOI:10.1155/2017/6848430