Cell penetrating recombinant Foxp3 protein enhances Treg function and ameliorates arthritis.
Cell penetrating recombinant Foxp3 protein enhances Treg function and ameliorates arthritis.
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DOI：
10.1016/j.bbrc.2013.02.114
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发表时间：
2013-05-03
影响因子：
3.1
通讯作者：
Chu, Cong-Qiu
中科院分区：
文献类型：
--
作者：
Yomogida, Kentaro;Wu, Shili;Baravati, Bobby;Avendano, Camilo;Caldwell, Tom;Maniaci, Brian;Zhu, Yong;Chu, Cong-Qiu
Foxp 3是调节性T细胞（Treg）分化和功能的主要转录因子。本研究旨在测试细胞穿透重组Foxp 3蛋白在关节炎中的治疗潜力。将重组Foxp 3蛋白与细胞穿透聚精氨酸（Foxp 3 - 11 R）标签融合以促进细胞内转导。与对照蛋白质处理的细胞相比，体外Foxp 3 - 11 R处理的CD 4 + T细胞显示出50%的抑制功能增加。Foxp 3 - 11 R处理的小鼠中关节炎的严重程度与用对照蛋白质处理的小鼠相比显著降低。来自Foxp 3 - 11 R处理的小鼠的淋巴结和脾脏的CD 4 + T细胞显示与对照蛋白处理的那些相比Foxp 3表达水平增加。这些结果表明，Foxp 3 - 11 R可以增强T细胞抑制功能，改善实验性关节炎，并表明细胞穿透重组Foxp 3是一个潜在的有用的药物在治疗关节炎。
Foxp3 is the master transcription factor for T regulatory (Treg) cell differentiation and function. This study aimed to test the therapeutic potential of cell penetrating recombinant Foxp3 protein in arthritis. Recombinant Foxp3 protein was fused to a cell penetrating polyarginine (Foxp3-11R) tag to facilitate intracellular transduction. In vitro Foxp3-11R treated CD4+ T cells showed a 50% increase in suppressive function compared with control protein treated cells. Severity of arthritis in Foxp3-11R treated mice was significantly reduced compared with those treated with a control protein. CD4+ T cells of lymph nodes and spleen from Foxp3-11R treated mice showed increased levels of Foxp3 expression compared with those of a control protein treated. These results demonstrated that Foxp3-11R can enhance T cell suppressive function and ameliorate experimental arthritis and suggest that cell penetrating recombinant Foxp3 is a potentially useful agent in therapy of arthritis.
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影响因子：
32.4
作者：
Fontenot, JD;Rasmussen, JP;Rudensky, AY
通讯作者：
Rudensky, AY
影响因子：
64.8
作者：
Sakaguchi, N;Takahashi, T;Sakaguchi, S
通讯作者：
Sakaguchi, S
影响因子：
3.8
作者：
Yomogida, Kentaro;Chou, Yuan;Chu, Cong-Qiu
通讯作者：
Chu, Cong-Qiu
影响因子：
14.2
作者：
Miyara, Makoto;Wing, Kajsa;Sakaguchi, Shimon
通讯作者：
Sakaguchi, Shimon
DOI：
10.4049/jimmunol.1003224
发表时间：
2011-09-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Long SA;Buckner JH
通讯作者：
Buckner JH