沙眼衣原体感染上皮细胞和树突状细胞导致IL-18和IL-12的产生,导致人类自然杀伤细胞产生干扰素-γ

Catherina Eliszbeth Hook, Malgosia K. Matyszak, John S. Hill Gaston
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引用次数: 44

摘要

控制沙眼衣原体感染通常需要产生干扰素-γ。虽然这可以由CD4+和CD8+ T淋巴细胞产生,但自然杀伤(NK)细胞是这种细胞因子的另一个重要来源,并且已知在感染生殖道的早期被招募。我们发现,在树突状细胞和上皮细胞感染后,分别产生协同刺激NK细胞产生干扰素γ的IL-12和IL-18,因为感染细胞的上清液可以替代重组细胞因子。这些结果表明,导致NK细胞产生干扰素-γ的条件将存在于感染部位,其中上皮细胞是感染的主要目标,上皮内的树突状细胞也可以进入细菌。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Infection of epithelial and dendritic cells by Chlamydia trachomatis results in IL-18 and IL-12 production, leading to interferon-γ production by human natural killer cells

Control of infection by Chlamydia trachomatis usually requires the production of interferon-γ. Whilst this can be produced by CD4+ and CD8+ T lymphocytes, natural killer (NK) cells are another important source of this cytokine, and are known to be recruited early to the infected genital tract. We show that both IL-12 and IL-18, which synergise to stimulate NK cells to produce interferon-γ, are produced following the infection of dendritic cells and epithelial cells respectively, since supernatants from infected cells could substitute for recombinant cytokines. These results suggest that conditions, which lead to NK cell production of interferon-γ will be present at the site of infection, where epithelial cells are the primary targets of infection and dendritic cells within the epithelium can also access the bacterium.

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