中文摘要：

目的探讨CD8＋T细胞在生理或病理性免疫应答中的免疫调节作用及其机制。方法将特异性CD8＋T细胞与骨髓体外诱导的或脾脏来源的树突状细胞（dendritic cells,DCs）共培养,检测DCs表面MHC-Ⅱ类分子和共刺激分子的表达;检测共培养后DCs刺激CD4＋T细胞增殖的能力。OVA致敏小鼠体内回输特异性CD8＋T细胞,分析CD8＋T细胞对脾脏DCs抗原递呈能力的影响;CD8＋T细胞干预后的致敏小鼠吸入OVA后,分析小鼠肺泡-支气管灌洗液（broncho-alveolar lavage fluid,BALF）中的白细胞和细胞因子,小鼠肺组织切片经HE和PAS染色观察其病理改变。结果 DCs与CD8＋T细胞共培养后,其MHC-Ⅱ类分子和共刺激分子的表达均下调,刺激CD4＋T细胞增殖能力显著下降;CD8＋T细胞体内回输后,小鼠脾脏DCs共刺激分子的表达及其刺激CD4＋T细胞增殖的能力均下调;与未干预组相比,CD8＋T细胞干预小鼠BALF中IL-4、IL-5质量浓度降低,肺部炎性细胞浸润和杯状细胞增生减少。结论特异性CD8＋T细胞活化可以通过下调DCs共刺激分子的表达来抑制DCs的抗原递呈能力,从而调节致敏CD4＋T细胞的增殖,缓解哮喘小鼠的症状。

英文摘要：

The purpose of this study is to investigate the immunoregulatory effects of activated CD8＋ T cells in pathological and physiological immune responses and the underlying mechanism. After co-cultivation with specific CD8＋T cells, BMDCs or spleen-derived DCs were analyzed for the expression of MHC-II and co-stimulatory molecules. Then CD8＋T cell-modified DCs were separated from the co-culture system and analyzed for their capacity to stimulate specific CD4＋T cell proliferation. C57BL/6 mice sensitized by OVA were intravenously infused with OVA257-264 specific CD8cr cells, and sacrificed 72 h after CD8＋T cell infusion for analyzing the expression levels of antigen-presentation-related molecules on splenic DCs as well as the capacity of the splenic DCs to stimulate CD4CF cell proliferation. After CDS＋T cells were infused into OVA-sensitized mice, recipient mice were challenged with aerosolized OVA daily for 30 min over 5 days, and were sacrificed 24 h after the last challenge. Bronchoalveolar lavage （BAL） was performed for analyzing the numbers of leukocytes and the levels of cytokines in BAL fluid （BALF）. The frozen sections of lung tissues were stained with hematoxylin and eosin （HE） and periodic acid- schiff stain （PAS） for analyzing pathological changes. We found that after co-cultivation with CD8＋T cells, DCs demonstrated decreases in the expression levels of MHC-II and co-stimulatory molecules and the capability to stimulate CD4＋T cell proliferation, while splenic DCs showed decreases in the expression of co-stimulatory molecules and the capacity to stimulate CD4＋T cell proliferation after CD8＋T cell infusion. When compared with the non-intervention mice, the inflammatory cell infiltration and concentrations of IL-4 and IL-5 in BALF were significantly decreased in CD8＋T cell intervention mice. In conclusion, our findings indicate that activated CD8＋T cells can exert a negative feedback on the antigen-presenting function of DCs, suggesting a potential mechanism that account