中文摘要：

目的 探讨白细胞介素22（IL-22）对异基因骨髓移植（allo-BMT）后并发移植物抗宿主病（GVHD）小鼠胸腺的修复作用及其对胸腺免疫功能的影响.方法 分别以6～8周龄、雄性C57BL/6和BALB/c小鼠为供受鼠,建立GVHD模型.实验分为正常对照组、GVHD小鼠注射IL-22组（BS＋IL-22）、GVHD小鼠注射PBS组（BS＋PBS）.采用锥虫蓝染色法检测移植后不同时间点小鼠胸腺细胞数量.采用流式细胞术检测胸腺T细胞各亚群的比例、分泌IFN-γ和IL-17效应性T细胞及CD4＋T和CD8＋T细胞比例.结果 ＋14d时BS＋IL-22组小鼠的胸腺细胞总数[（14.6±5.1）×10^4]明显高于BS＋PBS组[（6.2±2.9）×10^4];BS＋IL-22组小鼠胸腺细胞数量随移植时间延长持续增多,到＋21和＋28 d细胞数量与正常对照组小鼠相比差异无统计学意义,且仍高于BS＋PBS组.小鼠allo-BMT后注射IL-22对胸腺成熟CD4＋和CD8＋T细胞的比例无影响,但可显著提高未成熟CD4＋CD8＋T细胞亚群的比例.IL-22可上调胸腺IFN-γ＋CD4＋T细胞[（2.42±0.75）％]和IFN-γ＋CD8＋T细胞[（5.44±0.47）％]比例,而对IL-17＋CD4＋T细胞和IL-17＋CD8＋T细胞无影响.结论 IL-22可加速allo-BMT后小鼠胸腺的修复过程,并增强胸腺CD4＋和CD8＋T细胞分泌IFN-γ的能力.

英文摘要：

Objective To explore the role of IL-22 on the recovery and function of thymus from graft-versus host disease （GVHD） mice after allogeneic bone marrow transplantation （allo-BMT）.Methods GVHD model was established by using of recipient male BALB/c and donor male C57BL/6 mice （6-8 W） respectively.The mice were divided into normal group,GVHD with IL-22 group （BS＋ IL-22） and without IL-22 group （BS＋PBS）.Numbers of thymus cells were detected at different time points.The ratio of T cell subsets from thymus was observed by flow cytometry.Percentages of IFN-γ-producing and IL-17-producing CD4＋ T or CD8＋ T cells were detected.Results The total number of thymus cells in BS＋IL-22 mice [（14.6±5.1） × 10^4] was significantly higher than that in BS＋PBS mice [（6.2±2.9） × 10^4] at 14 days after allo-BMT.Thymus cells in BS＋IL-22 mice expanded continuously and reached at the level of normal mice,which were still higher than that in BS＋PBS group.Although there was no impact on the ratio of mature CD4＋ and CD8＋T cell from thymus,the percentage of immature CD4＋CD8＋T cell increased obviously in mice treated with IL-22.Percentages of IFN-γ＋CD4＋ T cell [Th1：（2.42±0.75） %] and IFN-γ＋CD8 ＋ T cell [Tc 1：（5.44±0.47） %] were up-regulated by IL-22 treatment,whereas no changes were detected in IL-17＋CD4＋ T cell（Th17）and IL-17＋CD8＋ T cell （Tc17）.Conclusions IL-22 accelerates the progress of thymus recovery,and increases the IFN-γ-producing ability of thymus CD4＋ and CD8＋ T cells from GVHD mice.