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首页> 外文期刊>Infection and immunity >Immunity to Chlamydia trachomatis Mouse Pneumonitis Induced by Vaccination with Live Organisms Correlates with Early Granulocyte-Macrophage Colony-Stimulating Factor and Interleukin-12 Production and with Dendritic Cell-Like Maturation
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Immunity to Chlamydia trachomatis Mouse Pneumonitis Induced by Vaccination with Live Organisms Correlates with Early Granulocyte-Macrophage Colony-Stimulating Factor and Interleukin-12 Production and with Dendritic Cell-Like Maturation

机译:接种活体疫苗对沙眼衣原体小鼠肺炎的免疫性与早期粒细胞-巨噬细胞集落刺激因子和白细胞介素12产生以及树突状细胞样成熟有关。

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As is true for other intracellular pathogens, immunization with live Chlamydia trachomatis generally induces stronger protective immunity than does immunization with inactivated organism. To investigate the basis for such a difference, we studied immune responses in BALB/c mice immunized with viable or UV-killed C. trachomatis mouse pneumonitis (MoPn). Strong, acquired resistance to C. trachomatis infection was elicited by immunization with viable but not dead organisms. Immunization with viable organisms induced high levels of antigen-specific delayed-type hypersensitivity (DTH), gamma interferon production, and immunoglobulin A (IgA) responses. Immunization with inactivated MoPn mainly induced interleukin-10 (IL-10) production and IgG1 antibody without IgA or DTH responses. Analysis of local early cytokine and cellular events at days 3, 5, and 7 after peritoneal cavity immunization showed that high levels of granulocyte-macrophage colony-stimulating factor and IL-12 were detected with viable but not inactivated organisms. Furthermore, enrichment of a dendritic cell (DC)-like population was detected in the peritoneal cavity only among mice immunized with viable organisms. The results suggest that early differences in inducing proinflammatory cytokines and activation and differentiation of DCs may be the key mechanism underlying the difference between viable and inactivated organisms in inducing active immunity to C. trachomatisinfection.
机译:与其他细胞内病原体一样,活沙眼衣原体免疫接种通常会比灭活生物体免疫接种产生更强的保护性免疫。为了研究这种差异的基础,我们研究了用活的或紫外线杀死的 C免疫的BALB / c小鼠的免疫应答。沙眼鼠肺炎(MoPn)。获得的对 C的强大抵抗力。沙眼菌感染是通过用有生命力的微生物(而非死生物)免疫引起的。活生物体的免疫诱导了高水平的抗原特异性迟发型超敏反应(DTH),γ干扰素产生和免疫球蛋白A(IgA)反应。灭活的MoPn免疫主要诱导白介素10(IL-10)产生和IgG1抗体,而没有IgA或DTH反应。对腹膜腔免疫后第3、5和7天的局部早期细胞因子和细胞事件的分析表明,在有活力但未灭活的生物体中检测到高水平的粒细胞-巨噬细胞集落刺激因子和IL-12。此外,仅在用活生物体免疫的小鼠中,腹膜腔中检测到树突状细胞(DC)样种群的富集。结果表明,诱导促炎细胞因子的早期差异以及DC的激活和分化可能是导致活菌和灭活生物体之间差异的关键机制,这些差异导致了对C的主动免疫。沙眼菌感染。

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