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Elicitation of Mucosal Immunitf by Proteins of Streptococcus pneumoniae

机译:链球菌蛋白蛋白蛋白的粘膜免疫诱导

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Pneumococcal diseases such as otitis media, pneumonia, and meningitis are invariably preceded by nasopharyn-geal colonization, and herd immunity against pneumococcal disease requires protection against colonization. An early study in mice demonstrated that mucosal immunization with cholera toxin B subunit as adjuvant could elicit solid mucosal immunity. Recent data from several laboratories provides support for three different mechanisms by which adaptive immunity can provide protection against colonization. (1) IL-17-dependent T cell immunity can recruit PMN to sites of colonization. This IL-17-dependent immunity can be elicited by immunization with antigen plus a mucosal adjuvant, or can be elicited by colonization itself. (2) Immunity against colonization can be mediated by mucosal IgA and at the mucosal surface passive mucosal IgA antibody provides much better protection against carriage than passive IgG antibody. (3) Complement-fixing IgG antibody can protect against colonization and may act by protecting against colonization of bacteria.
机译:肺炎患儿,脑膜炎和脑膜炎等肺炎球菌疾病在鼻咽 - 胚芽殖民化之前是不定期的,而患有针对肺炎球菌病的畜群免疫需要防止殖民化。小鼠的早期研究表明,作为佐剂B亚基的粘膜免疫,作为佐剂可以引起固体粘膜免疫。来自若干实验室的最近数据为三种不同机制提供了支持,自适应免疫可以提供针对殖民化的保护。 (1)IL-17依赖性T细胞免疫可以招募PMN到定植点。通过用抗原加上粘膜佐剂免疫,可以引发这种IL-17依赖性免疫,或者可以通过定植本身引发。 (2)针对定植的免疫可以通过粘膜IgA和粘膜表面介导,在粘膜表面无源粘膜IgA抗体比被动IgG抗体提供更好地保护。 (3)补体固定IgG抗体可以防止殖民化,并可通过保护细菌的定植来保护。

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