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首页> 外文期刊>Infection and immunity >Signaling via Interleukin-4 Receptor α Chain Is Required for Successful Vaccination against Schistosomiasis in BALB/c Mice
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Signaling via Interleukin-4 Receptor α Chain Is Required for Successful Vaccination against Schistosomiasis in BALB/c Mice

机译：要成功接种BALB / c小鼠血吸虫病，需要通过IL-4受体α链进行信号传递

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Although protective immunity in C57BL/6 mice induced by a single dose of the radiation-attenuated schistosome vaccine is believed to be mediated by Th1-type immune responses, we here report that in BALB/c mice protection can also depend upon signaling via the interleukin-4 (IL-4) receptor which conventionally governs the development of Th2-type immune responses. We show that in BALB/c mice deficient for the IL-4 receptor α chain (IL-4Rα?/?), which are unresponsive to IL-4 and IL-13, vaccine-induced protection is abrogated compared with that in wild-type (WT) mice. In vaccinated IL-4Rα?/? mice, IL-12p40 production by cells from the skin exposure site was elevated, although gamma interferon (IFN-γ) production in draining lymphoid tissues was similar in WT and IL-4Rα?/? mice. Nevertheless, the effector response in IL-4Rα?/? mice was Th1 biased with elevated IFN-γ in the lungs and higher immunoglobulin G2a (IgG2a) and IgG2b titers but negligible quantities of Th2-associated IgG1 and IgE. Interestingly, levels of IL-4 were equivalent in WT and IL-4Rα?/?mice, indicating that Th2 responses were not dependent upon signaling by IL-4 or IL-13. No differences in the phenotype and composition of the pulmonary effector mechanism that might explain the failure to induce protection in IL-4Rα?/? mice were detected. However, passive transfer of partial protection to naive IL-4Rα?/? mice, using serum from vaccinated WT mice, indicates that Th2-associated antibodies such as IgG1 have a role in parasite elimination in BALB/c strain mice and that signaling via IL-4R can be an important factor in the generation of protection.
机译：尽管据信由单剂量辐射减弱的血吸虫疫苗诱导的C57BL / 6小鼠的保护性免疫是由Th1型免疫应答介导的，但我们在此报告，在BALB / c小鼠中，保护也可能取决于通过白介素的信号传导-4（IL-4）受体，通常控制Th2型免疫应答的发展。我们显示，在对IL-4和IL-13无反应的IL-4受体α链（IL-4Rα？/？）缺失的BALB / c小鼠中，疫苗诱导的保护作用为与野生型（WT）小鼠相比废除。在接种过IL-4Rαα/β的小鼠中，皮肤暴露部位细胞分泌的IL-12p40有所增加，尽管引流淋巴组织中的γ-干扰素（IFN-γ）的产生与WT和IL相似-4Rα？/？小鼠。然而，IL-4Rα？/？小鼠中的效应反应是Th1偏向于肺中升高的IFN-γ和更高的免疫球蛋白G2a（IgG2a）和IgG2b滴度，但是与Th2相关的IgG1和IgE。有趣的是，WT-4和IL-4Rαα/β小鼠中IL-4的水平相等，表明Th2应答不依赖于IL-4或IL-13的信号传导。没有发现在肺效应器机制的表型和组成上的差异可以解释在IL-4Rα？/？小鼠中诱导保护失败的原因。然而，使用疫苗接种的WT小鼠血清将部分保护被动转移至幼稚IL-4Rαα/β小鼠，表明Th2相关抗体（例如IgG1）在BALB / c的寄生虫清除中具有作用小鼠和通过IL-4R的信号传导可能是产生保护作用的重要因素。

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