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首页> 外文期刊>Infection and immunity >Adenylate Cyclase Toxin from Bordetella pertussis Synergizes with Lipopolysaccharide To Promote Innate Interleukin-10 Production and Enhances the Induction of Th2 and Regulatory T Cells
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Adenylate Cyclase Toxin from Bordetella pertussis Synergizes with Lipopolysaccharide To Promote Innate Interleukin-10 Production and Enhances the Induction of Th2 and Regulatory T Cells

机译：百日咳博德氏杆菌的腺苷酸环化酶毒素与脂多糖协同作用，促进先天性白细胞介素10的产生，并增强对Th2和调节性T细胞的诱导

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Adenylate cyclase toxin (CyaA) from Bordetella pertussis can subvert host immune responses allowing bacterial colonization. Here we have examined its adjuvant and immunomodulatory properties and the possible contribution of lipopolysaccharide (LPS), known to be present in purified CyaA preparations. CyaA enhanced antigen-specific interleukin-5 (IL-5) and IL-10 production and immunoglobulin G1 antibodies to coadministered antigen in vivo. Antigen-specific CD4+-T-cell clones generated from mice immunized with antigen and CyaA had cytokine profiles characteristic of Th2 or type 1 regulatory T (Tr1) cells. Since innate immune cells direct the induction of T-cell subtypes, we examined the influence of CyaA on activation of dendritic cells (DC) and macrophages. CyaA significantly augmented LPS-induced IL-6 and IL-10 and inhibited LPS-driven tumor necrosis factor alpha and IL-12p70 production from bone marrow-derived DC and macrophages. CyaA also enhanced cell surface expression of CD80, CD86, and major histocompatibility class II on immature DC. The stimulatory activity of our CyaA preparation for IL-10 production and CD80, CD86, and major histocompatibility complex class II expression was attenuated following the addition of polymyxin B or with the use of DC from Toll-like receptor (TLR) 4-defective mice. However, treatment of DC with LPS alone at the concentration present in the CyaA preparation (0.2 ng/ml) failed to activate DC in vitro. Our findings demonstrate that activation of innate cells in vitro by CyaA is dependent on a second signal through a TLR and that CyaA can promote Th2/Tr1-cell responses by inhibiting IL-12 and promoting IL-10 production by DC and macrophages.
机译：百日咳博德特氏菌的腺苷酸环化酶毒素（CyaA）可以破坏宿主的免疫反应，使细菌得以定殖。在这里，我们检查了其佐剂和免疫调节特性以及已知存在于纯化的CyaA制剂中的脂多糖（LPS）的可能作用。 CyaA增强了抗原特异性白介素5（IL-5）和IL-10的产生以及免疫球蛋白G1抗体在体内共同施用的抗原。从抗原和CyaA免疫小鼠产生的抗原特异性CD4 + -T细胞克隆具有Th2或1型调节性T（Tr1）细胞特征的细胞因子特征。由于先天免疫细胞指导T细胞亚型的诱导，我们研究了CyaA对树突状细胞（DC）和巨噬细胞活化的影响。 CyaA显着增加了LPS诱导的IL-6和IL-10，并抑制了LPS驱动的肿瘤坏死因子α和IL-12p70从骨髓来源的DC和巨噬细胞中产生。 CyaA还增强了未成熟DC上CD80，CD86和主要组织相容性II类的细胞表面表达。加入多粘菌素B或使用Toll样受体（TLR）4缺陷小鼠的DC后，我们的CyaA制剂对IL-10产生以及CD80，CD86和主要组织相容性复合体II类表达的刺激活性减弱。 。但是，仅以CyaA制剂中存在的浓度（0.2 ng / ml）的LPS处理DC无法在体外激活DC。我们的发现表明，CyaA在体外对先天细胞的激活取决于通过TLR产生的第二个信号，并且CyaA可以通过抑制IL-12并促进DC和巨噬细胞的IL-10产生来促进Th2 / Tr1细胞反应。

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