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首页> 外文期刊>Infection and immunity >In the Absence of CD154, Administration of Interleukin-12 Restores Th1 Responses but Not Protective Immunity to Schistosoma mansoni
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In the Absence of CD154, Administration of Interleukin-12 Restores Th1 Responses but Not Protective Immunity to Schistosoma mansoni

机译：在没有CD154的情况下，白介素12的使用可恢复Th1反应，但对曼氏血吸虫没有保护性免疫

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The cytokine interplay during the development of protective immunity to the radiation-attenuated (RA) schistosome vaccine has been extensively characterized over recent years, yet the role of costimulatory molecules in the development of cell-mediated immunity is much less well understood. Here we demonstrate the importance of CD40/CD154 in vaccine-induced immunity, as CD154?/? mice exposed to RA schistosomes develop no protection to challenge infection. We showed that vaccinated CD154?/? mice have defective Th1-associated immune responses in the skin-draining lymph nodes and the lungs, with reduced or absent levels of interleukin-12p40 (IL-12p40), gamma interferon, and nitric oxide, but elevated levels of lung IL-4 and IL-5. The expression of major histocompatibility complex II (MHC-II) on antigen-presenting cells recovered from the lungs of vaccinated CD154?/? mice was also severely compromised. The administration of anti-CD40 monoclonal antibody (MAb) to CD154?/? mice did not reconstitute sustained Th1 responses in the lymph nodes or the lungs, nor did the MAb restore anti-parasite immunoglobulin G production or protective immunity. On the other hand, the administration of recombinant IL-12 (rIL-12) to CD154?/? mice shortly after vaccination caused elevated and sustained levels of Th1-associated cytokines, rescued MHC-II expression by lung CD11c+ cells, and restored the appearance of inflammatory effector foci in the lungs. However, the treatment of CD154?/? mice with rIL-12 did not restore protection. We conclude that protective immunity to the RA schistosome vaccine is CD154 dependent but is independent of IL-12-orchestrated cellular immune mechanisms in the lungs.
机译：近年来，对辐射减弱的（RA）血吸虫疫苗的保护性免疫发展过程中的细胞因子相互作用已得到了广泛的表征，然而，共刺激分子在细胞介导的免疫发展中的作用却鲜为人知。在这里，我们证明了CD40 / CD154在疫苗诱导的免疫中的重要性，因为暴露于RA血吸虫的CD154 ？/？小鼠对攻击没有形成保护作用。我们显示，接种CD154 ？/？的小鼠在引流皮肤的淋巴结和肺部具有缺陷的Th1相关免疫反应，其白介素12p40（IL-12p40），γ的水平降低或缺失干扰素和一氧化氮，但肺IL-4和IL-5水平升高。从接种的CD154 ？/？小鼠的肺中回收的抗原呈递细胞上的主要组织相容性复合物II（MHC-II）的表达也受到严重损害。向CD154 ？/？小鼠施用抗CD40单克隆抗体（MAb）不能重建淋巴结或肺中持续的Th1反应，MAb也不能恢复抗寄生虫免疫球蛋白G的产生或保护免疫力。另一方面，在接种疫苗后不久向CD154 ？/？小鼠施用重组IL-12（rIL-12）导致与Th1相关的细胞因子水平升高和持续，从而通过MHC-II表达得以拯救肺CD11c + 细胞，并恢复了肺部炎症效应灶的出现。然而，用rIL-12治疗CD154 α/β小鼠不能恢复保护。我们得出结论，对RA血吸虫疫苗的保护性免疫是CD154依赖性的，但独立于肺中IL-12调控的细胞免疫机制。

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