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

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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.