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Th1-Th17 cells mediate protective adaptive immunity against Staphylococcus aureus and Candida albicans infection in mice.Th1-Th17 细胞介导了小鼠对抗金黄色葡萄球菌和白色念珠菌感染的保护性适应性免疫。
PLoS Pathog. 2009 Dec;5(12):e1000703. doi: 10.1371/journal.ppat.1000703. Epub 2009 Dec 24.
2
Interleukin-17 regulates chemokine and gelatinase B expression in fibroblasts to recruit both neutrophils and monocytes.白细胞介素-17调节成纤维细胞中趋化因子和明胶酶B的表达,以募集嗜中性粒细胞和单核细胞。
Immunobiology. 2009;214(9-10):835-42. doi: 10.1016/j.imbio.2009.06.007. Epub 2009 Jul 22.
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Cellular effectors mediating Th17-dependent clearance of pneumococcal colonization in mice.介导小鼠肺炎球菌定植的Th17依赖性清除的细胞效应物。
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Differential roles of interleukin-17A and -17F in host defense against mucoepithelial bacterial infection and allergic responses.白细胞介素-17A和-17F在宿主抵御黏膜上皮细菌感染及过敏反应中的不同作用
Immunity. 2009 Jan 16;30(1):108-19. doi: 10.1016/j.immuni.2008.11.009.
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An overview of IL-17 function and signaling.白细胞介素-17的功能与信号传导概述。
Cytokine. 2008 Sep;43(3):402-7. doi: 10.1016/j.cyto.2008.07.017. Epub 2008 Aug 12.
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IFN-gamma regulated chemokine production determines the outcome of Staphylococcus aureus infection.γ干扰素调节趋化因子的产生决定了金黄色葡萄球菌感染的结果。
J Immunol. 2008 Jul 15;181(2):1323-32. doi: 10.4049/jimmunol.181.2.1323.
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The biological functions of T helper 17 cell effector cytokines in inflammation.辅助性T细胞17效应细胞因子在炎症中的生物学功能
Immunity. 2008 Apr;28(4):454-67. doi: 10.1016/j.immuni.2008.03.004.
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Induction of a distinct CD8 Tnc17 subset by transforming growth factor-beta and interleukin-6.转化生长因子-β和白细胞介素-6诱导出独特的CD8 Tnc17亚群。
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IL-17-mediated regulation of innate and acquired immune response against pulmonary Mycobacterium bovis bacille Calmette-Guerin infection.白细胞介素-17介导的针对肺部卡介苗感染的先天性和获得性免疫反应的调节
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白细胞介素-17A 在用凝聚因子 A 的纤维蛋白原结合结构域免疫的小鼠中对金黄色葡萄球菌感染的细胞介导保护作用。

Role of interleukin-17A in cell-mediated protection against Staphylococcus aureus infection in mice immunized with the fibrinogen-binding domain of clumping factor A.

机构信息

Department of Microbiology and Immunology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.

出版信息

Infect Immun. 2010 Oct;78(10):4234-42. doi: 10.1128/IAI.00447-10. Epub 2010 Aug 2.

DOI:10.1128/IAI.00447-10
PMID:20679443
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2950370/
Abstract

Clumping factor A (ClfA) is a fibrinogen-binding cell wall-attached protein and an important virulence factor of Staphylococcus aureus. Previous studies reported that an immunization with the fibrinogen-binding domain of ClfA (ClfA(40-559)) protected animals against S. aureus infection. It was reported that some cytokines are involved in the pathogenesis of staphylococcal diseases and in host defense against S. aureus infection. However, the role of cytokines in the protective effect of ClfA(40-559) as a vaccine has not been elucidated. In this study, we demonstrated that the spleen cells of ClfA(40-559)-immunized mice produced a large amount of interleukin-17A (IL-17A). The protective effect of immunization was exerted in wild-type mice but not in IL-17A-deficient mice. IL-17A mRNA expression was increased in the spleens and kidneys of immunized mice after infection. CXCL2 and CCL2 mRNA expression was increased in the spleens and kidneys, respectively. Consistent with upregulation of the mRNA expression, neutrophils infiltrated into the spleens extensively and macrophage infiltration was observed in the kidneys of immunized mice. These results suggest that immunization with ClfA(40-559) induces the IL-17A-producing cells and that IL-17-mediated cellular immunity is involved in the protective effect induced by immunization with ClfA(40-559) against S. aureus infection.

摘要

凝聚因子 A(ClfA)是一种纤维蛋白原结合的细胞壁附着蛋白,也是金黄色葡萄球菌的重要毒力因子。先前的研究表明,用 ClfA 的纤维蛋白原结合结构域(ClfA(40-559))免疫可以保护动物免受金黄色葡萄球菌感染。据报道,一些细胞因子参与了葡萄球菌病的发病机制以及宿主对金黄色葡萄球菌感染的防御。然而,细胞因子在 ClfA(40-559)作为疫苗的保护作用中的作用尚未阐明。在这项研究中,我们证明了 ClfA(40-559)免疫小鼠的脾细胞产生了大量的白细胞介素-17A(IL-17A)。免疫的保护作用仅在野生型小鼠中发挥,而在 IL-17A 缺陷型小鼠中则不发挥。感染后,免疫小鼠的脾脏和肾脏中 IL-17A mRNA 表达增加。脾脏和肾脏中分别增加了 CXCL2 和 CCL2 的 mRNA 表达。与 mRNA 表达的上调一致,大量中性粒细胞浸润到脾脏中,并且在免疫小鼠的肾脏中观察到巨噬细胞浸润。这些结果表明,用 ClfA(40-559)免疫可诱导产生产生 IL-17A 的细胞,并且 IL-17 介导的细胞免疫参与了用 ClfA(40-559)免疫诱导的针对金黄色葡萄球菌感染的保护作用。