BACKGROUND T lymphocytes play an important role in contact hypersensitivity. This study aims to explore the immunosuppressive activity of SBF-1, an analog of saponin OSW-1, against T lymphocytes in vitro and in vivo. METHODS Proliferation of T lymphocytes from lymph nodes of mice was determined by MTT assay. Flow cytometry analysis was performed to assess T cell activation and apoptosis. Levels of cytokines were determined by PCR and ELISA. BALB/c mice were sensitized and challenged with picryl chloride and thickness of left and right ears were measured. RESULTS SBF-1 effectively inhibited T lymphocytes proliferation induced by concanavalin A (Con A) or anti-CD3 plus anti-CD28 at a very low dose (10 nM) but exhibited little toxicity in non-activated T lymphocytes at concentrations up to 10 μM. In addition, SBF-1 inhibited the expression of CD25 and CD69, as well as he phosphorylation of AKT in Con A-activated T cells. SBF-1 also induced apoptosis of activated T cells. In addition, SBF-1 also downregulated the induction of the T cell cytokines, IL-2 and IFN-γ in a dose-dependent manner. Furthermore, SBF-1 significantly suppressed ear swelling and inflammation in a mouse model of picryl chloride-induced contact hypersensitivity. CONCLUSIONS Our findings suggest that SBF-1 has an unique immunosuppressive activity both in vitro and in vivo mainly through inhibiting T cell proliferation and activation. Its mechanism appears to be related to the blockage of AKT signaling pathway.

中文翻译：

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SBF-1通过下调T细胞介导的反应来抑制小鼠的接触超敏反应。

背景技术T淋巴细胞在接触超敏反应中起重要作用。这项研究旨在探讨SBF-1（皂苷OSW-1的类似物）在体外和体内对T淋巴细胞的免疫抑制活性。方法采用MTT法测定小鼠淋巴结中T淋巴细胞的增殖情况。进行流式细胞术分析以评估T细胞的活化和凋亡。通过PCR和ELISA确定细胞因子的水平。使BALB / c小鼠致敏并用氯化聚甲基吡啶攻击，并测量左耳和右耳的厚度。结果SBF-1在非常低的剂量（10 nM）下有效抑制了伴刀豆球蛋白A（Con A）或抗CD3加抗CD28诱导的T淋巴细胞增殖，但在浓度高达10μM的未激活T淋巴细胞中几乎没有毒性。此外，SBF-1抑制了Con A激活的T细胞中CD25和CD69的表达以及AKT的磷酸化。SBF-1还诱导活化的T细胞凋亡。此外，SBF-1还以剂量依赖性方式下调了T细胞细胞因子，IL-2和IFN-γ的诱导。此外，SBF-1在氯化聚氯化吡啶诱导的接触性超敏反应的小鼠模型中显着抑制了耳朵肿胀和炎症。结论我们的发现表明SBF-1在体外和体内均具有独特的免疫抑制活性，主要是通过抑制T细胞的增殖和活化来实现的。其机制似乎与AKT信号通路的阻断有关。SBF-1还以剂量依赖性方式下调了T细胞细胞因子，IL-2和IFN-γ的诱导。此外，SBF-1在氯化聚氯化吡啶诱导的接触性超敏反应的小鼠模型中显着抑制了耳朵肿胀和炎症。结论我们的发现表明SBF-1在体外和体内均具有独特的免疫抑制活性，主要是通过抑制T细胞的增殖和活化来实现的。其机制似乎与AKT信号通路的阻断有关。SBF-1还以剂量依赖性方式下调了T细胞细胞因子，IL-2和IFN-γ的诱导。此外，SBF-1在氯化聚氯化吡啶诱导的接触性超敏反应的小鼠模型中显着抑制了耳朵肿胀和炎症。结论我们的发现表明SBF-1在体外和体内均具有独特的免疫抑制活性，主要是通过抑制T细胞的增殖和活化来实现的。其机制似乎与AKT信号通路的阻断有关。结论我们的发现表明SBF-1在体外和体内均具有独特的免疫抑制活性，主要是通过抑制T细胞的增殖和活化来实现的。其机制似乎与AKT信号通路的阻断有关。结论我们的发现表明SBF-1在体外和体内均具有独特的免疫抑制活性，主要是通过抑制T细胞的增殖和活化来实现的。其机制似乎与AKT信号通路的阻断有关。