Increasing rates of life-threatening infections and decreasing susceptibility to antibiotics urge an effective vaccine targeting Staphylococcus aureus. Here we investigate the role of cellular immunity in FnBPA_110–263 mediated protection in Staphylococcus aureus infection. This study revealed FnBPA_110–263 broadly protected mice from seven FnBPA isotypes strains in the sepsis model. FnBPA_110–263 immunized B-cell deficient mice were protected against lethal challenge, while T-cell deficient mice were not. Reconstituting mice with FnBPA_110–263 specific CD4+ T-cells conferred antigen specific protection. In vitro assays indicated that isolated FnBPA_110–263 specific splenocytes from immunized mice produced abundant IL-17A. IL-17A deficient mice were not protected from a lethal challenge by FnBPA_110–263 vaccination. Moreover, neutralizing IL-17A, but not IFN-γ,reverses FnBPA_110–263-induced protective efficacy in sepsis and skin infection model. These findings suggest that IL-17A producing Th17 cells play an essential role in FnBPA_110–263 vaccine-mediated defense against S. aureus sepsis and skin infection in mice.

提高威胁生命的感染率和对抗生素的敏感性降低，促使针对金黄色葡萄球菌的有效疫苗问世。在这里，我们研究了细胞免疫在金黄色葡萄球菌感染中FnBPA _110-263介导的保护中的作用。这项研究表明，脓毒症模型中FnBPA _110-263对7种FnBPA同种型的小鼠_具有广泛的保护作用。FnBPA _110-263免疫的B细胞缺陷小鼠受到了致命性攻击的保护，而T细胞缺陷小鼠则没有。用FnBPA _110-263特异性CD4 + T细胞重建小鼠具有抗原特异性保护作用。体外测定表明，分离出的FnBPA _110–263来自免疫小鼠的特异性脾细胞产生大量的IL-17A。IL-17A缺陷小鼠不能通过_{FnBPA 110-263}疫苗免于致命攻击。此外，中和IL-17A，而不是IFN-γ，可以逆转FnBPA _110-263诱导的败血症和皮肤感染模型的保护作用。这些发现表明，产生IL-17A的Th17细胞在FnBPA _110-263疫苗介导的抗金黄色葡萄球菌败血症和小鼠皮肤感染的防御中起着至关重要的作用。