中文摘要：

为探讨I型调节性T细胞（Tr1）与CD4^＋CD25^＋Foxp3^＋Treg之间的转化和相互关系，以预包被而固相化的B7H1-lg融合蛋白加抗CD3单抗刺激初始CD4^＋CD62L^＋T细胞，分析细胞因子及Foxp3表达水平的变化，检测细胞功能；在B7H1-Ig开始刺激时或诱导细胞分化结束后加入重组人TGF-β，观察其对细胞分化的影响。结果显示，B7H10Ig激活的CD4^＋T细胞产生高水平IL-10、IFN-γ和IL-5，极低水平的IL-2和IL-4，不表达Foxp3，通过分泌抑制性细胞因子IL-10发挥免疫抑制功能，证实B7H1-Ig可诱导Tr1细胞的产生。同时发现TGF-β 不影响B7HI-Ig刺激的初始CD4^＋T的分化，却可促进B7H1-Ig诱导的已分化Tr1细胞向CD4^＋CD25^＋Foxp3^＋Treg转化，提示在特定条件下，Tr1细胞可转化的CD4^＋CD25^＋Foxp3^＋Treg。研究结果为将来临床应用CD4^＋Treg治疗免疫失调性疾病奠定了基础。

英文摘要：

To investigate the transfomation and relationship between type 1 regulatory T cells（Trl） and CD4^＋ CD25^＋ Foxp3^＋Tregs, isolated naive CD4^＋ CD62L^＋ T cells were stimulated with plate-bound B7HI-Ig plus anti-CD3, then the expression levels of cytokines and Foxp3 were analyzed, and the function of the resulting T cells were detected. Recombinant human （rh） TGF-13 was added at the time of culture initation or after stimulation to observe how it affected the differentiation of CD4^＋ T cells in the culture. Our results showed that B7Hl-Ig-activated CD4^＋T cells had the following characteristics.. They produced high levels of IL-10, IFN-γ and IL-5 and a very low level of IL-2 and IL-4. They didn＇t express the transcription factor Foxp3, but played immunosuppressive roles by secreting IL-10. These results demonstrate that B7HI-Ig can induce the generation of Trl cells. It was also found that TGF-β had no effect on the differentiation of BTHl-Ig-stimulated naive CD4^＋ T cells, but it could promote the B7Hl-stimulated, fully differentiated Trl cells to transform into CD4^＋ CD25^＋ Foxp3^＋ Tregs. These findings strongly suggest that Trl cells can transform into CD4^＋ CD25^＋ Foxp3^＋ Treg cells under certain conditions. Our study might be helpful to facilitate the using of CD4^＋ Treg for treatment of diseases caused by immunological disregulation.