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目的 研究天花粉蛋白 (Tk)诱导免疫抑制的免疫学机制。方法 应用淋巴细胞体外增殖抑制试验 ,分别对丝裂原ConA、可溶性抗原OVA及CD3联合CD2 8McAb三种T细胞增殖系统进行Tk诱导免疫抑制的剂量依赖性试验。建立OVA特异性的T细胞系 (Tova) ,观察Tk对由IL 2 IL 2R信号介导的T细胞增殖的抑制作用。用FACS测定Tk处理过的脾脏单个核细胞 (SMC)的凋亡。分离骨髓诱导产生未成熟的DC(iBDC) ,比较Tk冲击处理前后DC激活T细胞增殖能力的差异。用Tk冲击处理Tova ,观察Tk冲击处理前后T细胞增殖能力的变化。结果 低剂量的Tk(1ng ml～ 5 0 0ng ml)对OVA增殖系统有强烈的抑制作用 ,对ConA增殖系统抑制较弱 ,而对CD3联合CD2 8McAb及IL 2增殖系统的T细胞增殖几乎无抑制作用。在 5 μg ml的浓度以下 ,Tk不诱导SMC凋亡。Tk冲击处理过的iBDC提呈OVA激活特异性T细胞的能力明显下降 ;而Tk冲击处理过的Tova增殖能力没有受到影响。结论 Tk通过影响APC来诱导免疫抑制。
Objective To study the immunological mechanism of induced immunosuppression by trichosanthin (Tk). Methods The lymphocyte proliferation inhibition assay was performed in vitro. The Tk induced immunosuppressive effects of mitogen ConA, soluble antigen OVA and CD3 combined with CD28 8 McAb were tested in a dose-dependent manner. An OVA-specific T cell line (Tova) was established and the inhibitory effect of Tk on T cell proliferation mediated by IL 2 IL 2R signaling was observed. The apoptosis of Tk-treated splenic mononuclear cells (SMC) was measured by FACS. Isolation of bone marrow induced immature DCs (iBDCs) to compare differences in the ability of DC-activated T cells to proliferate before and after Tk shock treatment. Tova treatment was performed with Tk shock to observe the changes of T cell proliferation ability before and after Tk shock treatment. Results Low-dose Tk (1 ng ml to 500 ng ml) strongly inhibited the OVA proliferation system, inhibited the proliferation of ConA, and showed little inhibition of the proliferation of CD3 plus CD28 8 McAb and IL-2 proliferating system. effect. At concentrations below 5 μg ml, Tk did not induce SMC apoptosis. The ability of Tk-treated iBDCs to elicit specific activation of specific T cells by OVA was significantly reduced, whereas the proliferation of Tk-treated Tova was not affected. Conclusion Tk induces immunosuppression by affecting APC.