IFN-γ 缺陷使裸鼠的卡氏肺孢子虫肺炎加重，伴有 Th17 细胞的发展。
IFN-gamma deficiency worsen Pneumocystis pneumonia with Th17 development in nude mice.
机构信息
Department of Infection and Host Defense, Shinshu University Graduate School of Medicine, Asahi 3-1-1, Matsumoto 390-8621, Japan.
出版信息
Immunol Lett. 2009 Dec 2;127(1):55-9. doi: 10.1016/j.imlet.2009.08.013. Epub 2009 Sep 4.
Pneumocystis pneumonia (PCP) occurs frequently in patients with immunodeficiency syndromes, especially AIDS. In order to investigate the role of IFN-gamma on PCP, nude mice deficient in IFN-gamma (GKO nude) and their wild-type ones (WT nude) were infected with murine Pneumocystis. Nine weeks later they were sacrificed, and cytokines in BALF and lung histopathology were compared between them. Cyst burden was greater in GKO than in WT nude mice. Histopathology in the lung was severer and granulomatous lesions were observed more frequently in GKO nude mice. Levels of IL-17 were higher in BALF of GKO than in that of WT nude mice. Greater number of CD4(+) T cells from lungs of infected GKO nude mice produced IL-17 than those from WT ones. These results suggest that deficiency in IFN-gamma induces the differentiation of Th17 and that IL-17 is responsible for inflammatory response in PCP.
卡氏肺孢子虫肺炎（PCP）常发生于免疫缺陷综合征患者，尤其是艾滋病患者。为了研究 IFN-γ 在 PCP 中的作用，我们用鼠卡氏肺孢子虫感染 IFN-γ 缺陷型（GKO 裸鼠）及其野生型（WT 裸鼠）。9 周后处死它们，比较 BALF 和肺组织病理学中的细胞因子。GKO 裸鼠中的囊泡负荷比 WT 裸鼠更高。GKO 裸鼠的肺组织病理学更严重，并且更常观察到肉芽肿病变。GKO 裸鼠 BALF 中的 IL-17 水平高于 WT 裸鼠。来自感染 GKO 裸鼠肺部的 CD4+T 细胞比来自 WT 裸鼠的细胞产生更多的 IL-17。这些结果表明 IFN-γ 缺乏诱导 Th17 的分化，而 IL-17 是 PCP 中炎症反应的原因。
Zotero 插件