中文摘要：

目的 探讨重组人白介素23（IL-23）是否能够诱导正常人T细胞IFN-γ的产生，作用的靶细胞亚群和调节因素。方法 正常人PBMC在抗CD3（anti-CD3）单克隆抗体或anti-CD3和抗CD28（anti-CD28）单克隆抗体刺激的条件下与IL-23进行培养，采用酶联免疫吸附试验（ELISA）检测细胞培养液中IFN-γ的水平；同时采用流式细胞仪，在单个细胞水平上分析IL-23诱导PBMC IFN-γ表达的T细胞亚群。结果 在未经任何刺激的情况下，PBMC产生很低或不产生IFN-γ。IL-23呈剂量依赖方式促进由anti-CD3活化的PBMC IFN-γ产生。细胞亚群分析的结果表明，IL-23诱导记忆CD4^＋和CD8^＋T细胞表达IFN-γ，对活化的CD4^＋T细胞作用较为明显。Th2细胞因子（IL-4、IL-10）和抗IL-12受体β1 mAb（IL-12Rβ1）抑制IL-23诱导T细胞IFN-γ产生。结论 IL-23促进活化的记忆CD4^＋和CD8^＋T细胞IFN-γ的产生。Th2细胞因子和抗IL-12Rβ1 mAb抑制由IL-23诱导IFN-γ产生，提示这些细胞因子和抗体对IL-23引起的自身免疫病具有拮抗作用。

英文摘要：

Objective To evaluate the role of IL-23 in the IFN-γ production by activated human peripheral blood mononuclear cells （PBMCs）. Methods PBMCs were isolated from normal human peripheral blood and cultured with anti-CD3 mAb or anti-CD3 plus anti-CD28 mAb in the presence or absence of IL-23. The level of IFN-γ in the culture supernatants was assessed by ELISA. The subsets and frequency of IFN-γ-producing cells were examined at a single cell level by flow cytometry. Results IL-23 enhanced IFN-γ production by anti-CD3- or anti- CD3 plus anti-CD28 mAb-stimulated PBMCs in a dose-dependent manner. The data from flow cytometric analysis indicated that IL-23 could enhance IFN-γ expression by activated memory CD4^＋ and CD8^＋ T cells. Addition ofTh2 cytokines （IL-4 and IL-10） or anti-IL-12Rβ1 mAbs resulted in the inhibition of IL-23-inducing IFN-γ production. Conclusion IL-23 could promote IFN-γ production by activated memory T cells. The production of IFN-γ induced by IL-23 can be suppressed by Th2 cytokines and anfi-IL-12Rβ1 mAbs, indicating that Th2 cytokines and antiIL-12Rβ1 mAbs might have the potential application for the treatment of IL-23-mediated antoimmune diseases.