Trypanosoma cruzi (Y strain)-infected interleukin-4(-/-) (IL-4(-/-)) mice of strains 129/J, BALB/c, and C57BL/6 showed no significant difference in parasitemia levels or end point mortality rates compared to wild-type (WT) mice. Higher production of gamma interferon (IFN-gamma) by parasite antigen (Ag)-stimulated splenocytes was observed only for C57BL/6 IL-4(-/-) mice. Treatment of 129/J WT mice with recombinant IL-4 (rIL-4), rIL-10, anti-IL-4, and/or anti-IL-10 monoclonal antibodies (MAbs) did not modify parasitism. However, WT mice treated with rIL-4 and rIL-10 had markedly increased parasitism and suppressed IFN-gamma synthesis by spleen cells stimulated with parasite Ag, concanavalin A, or anti-CD3. Addition of anti-IL-4 MAbs to splenocyte cultures from infected WT 129/J, BALB/c, or C57BL/6 mice failed to modify IFN-gamma synthesis levels; in contrast, IL-10 neutralization increased IFN-gamma production and addition of rIL-4 and/or rIL-10 diminished IFN-gamma synthesis. We conclude that endogenous IL-4 is not a major determinant of susceptibility to Y strain T. cruzi infection but that IL-4 can, in association with IL-10, modulate IFN-gamma production and resistance.

译文

克氏锥虫 (Y株) 感染的interleukin-4(-/-) (IL-4(-/-)) 129/J,BALB/c和C57BL/6株小鼠与野生型 (WT) 小鼠相比,寄生虫血症水平或终点死亡率没有显着差异。仅在C57BL/6 IL-4(-/-) 小鼠中观察到由寄生虫抗原 (Ag) 刺激的脾细胞产生的较高 γ 干扰素 (IFN-γ)。用重组IL-4 (rIL-4) 、rIL-10、anti-IL-4和/或anti-IL-10单克隆抗体 (mab) 处理129/jwt小鼠不会改变寄生虫。然而,用rIL-4和rIL-10处理的WT小鼠的寄生虫显着增加,并抑制了被寄生虫Ag,伴刀豆球蛋白A或anti-CD3刺激的脾细胞的IFN-γ 合成。向感染的WT 129/J、BALB/c或C57BL/6小鼠的脾细胞培养物中添加anti-IL-4 mab不能改变IFN-γ 的合成水平; 相反,IL-10中和增加IFN-γ 的产生和添加rIL-4和/或rIL-10减少IFN-γ 的合成。我们得出的结论是,内源性IL-4不是Y株T. cruzi感染易感性的主要决定因素,但IL-4可以与IL-10相关地调节IFN-γ 的产生和抗性。

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