Differential function of antigen-presenting cells induced by IL-3 in host protective immunity against Trichinella spiralis infection

我们已经报道，旋毛虫感染后用rIL-3治疗的小鼠的Th2反应和保护性免疫都被加速。目前尚不清楚IL-3如何在感染早期使宿主免疫系统倾向于Th2优势。在本研究中，我们分析了能够同时传递保护性免疫和Th2反应的细胞，这些细胞可以传递给幼年C3H/He小鼠。分离经rIL-3处理的小鼠脾细胞。细胞移植后一天，用400只旋毛虫肌幼虫攻击小鼠。结果表明，细胞转移诱导的保护性免疫依赖于细胞转移的数量。将脾细胞培养在塑料培养皿中，贴壁细胞可将免疫传递给正常小鼠，而非贴壁细胞则不能。此外，我们用抗CD11b和抗CD45R的单抗分离细胞。CD11b+细胞移植组小鼠的成虫负担明显低于对照组。在抗CD3单抗刺激下分离和培养小鼠脾细胞。我们测定了细胞培养上清液中的细胞因子。CD11b+细胞转染组小鼠脾细胞产生IL-4的能力明显高于对照组。CD11b+细胞移植组小鼠的IL-2水平虽无明显差异，但产生IL-10的能力较弱。提示IL-3作用于CD11b+细胞，通过Th2细胞因子的差异表达调节旋毛虫感染小鼠的保护性免疫。

We have reported that both Th2 responses and protective immunity were accelerated in mice treated with rIL-3 after an infection of Trichinella spiralis. It has been unclear how IL-3 predisposes the host's immune system to Th2 dominance in the early stage of the infection. In the present study, we analyzed the cells that could transfer both protective immunity and Th2 responses to naive C3H/He mice. The spleen cells were isolated from mice treated with rIL-3. One day after the cell transfer, mice were challenged with 400 muscle larvae of T.spiralis. The result showed that protective immunity induced by the cell transfer was dependent on the number of the cells transferred. When the spleen cells were incubated in plastic petri dishes, adherent cells could transfer the immunity to normal mice but not non-adherent cells. Furthermore, we separated the cells, using anti-CD11b and anti-CD45R monoclonal antibodies(mAbs). Adult worm burden in mice transferred with CD11b_+ cells was significantly less than that in control. Spleen cells of the challenged mice were isolated and cultured under the stimulation of anti-CD3 mAb. We measured cytokines in the supernatant of the cell culture. IL-4 production in spleen cells from mice transferred with CD11b_+ cells was significantly higher than that of control. Although there was no significant difference of IL-2 among the groups, the cells from mice transferred with CD11b_+ cells produced less IL-10. These results suggest that IL-3 acts on CD11b_+ cells and regulates protective immunity through differential expression of Th2 cytokines in mice infected with T.spiralis.