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实验性盘尾丝虫性角膜炎(河盲症)的发展需要白细胞介素4和2型辅助性T细胞。

Interleukin 4 and T helper type 2 cells are required for development of experimental onchocercal keratitis (river blindness).

作者信息

Pearlman E, Lass J H, Bardenstein D S, Kopf M, Hazlett F E, Diaconu E, Kazura J W

机构信息

Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA.

出版信息

J Exp Med. 1995 Oct 1;182(4):931-40. doi: 10.1084/jem.182.4.931.

Abstract

Inflammation of the corneal stroma (stromal keratitis) is a serious complication of infection with the nematode parasite Onchocerca volvulus. Because stromal keratitis is believed to be immunologically mediated in humans, we used a murine model to examine the role of T cells and T helper cell cytokines in the immunopathogenesis of these eye lesions. BALB/c mice immunized subcutaneously and injected intrastromally with soluble O. volvulus antigens (OvAg) developed pronounced corneal opacification and neovascularization. The corneal stroma was edematous and contained numerous eosinophils and mononuclear cells. Stromal keratitis in immunized mice was determined to be T cell dependent based on the following observations: (a) T cell-deficient nude mice immunized and injected intrastromally with OvAg fail to develop corneal pathology; and (b) adoptive transfer of spleen cells from OvAg-immunized BALB/c mice to naive nude mice before intrastromal injection of OvAg results in development of keratitis. OvAg-stimulated lymph node and spleen cell cytokine production was dependent on CD4 cells and included interleukin (IL)-4 and IL-5, but not interferon gamma, indicating a predominant T helper type 2 cell-like response. Inflamed corneas from immunized BALB/c mice and from reconstituted nude mice had greatly elevated CD4 and IL-4 gene expression compared with interferon gamma. Mice in which the IL-4 gene was disrupted failed to develop corneal disease, demonstrating that IL-4 is essential in the immunopathogenesis of O. volvulus-mediated stromal keratitis.

摘要

角膜基质炎(基质性角膜炎)是盘尾丝虫线虫寄生虫感染的一种严重并发症。由于基质性角膜炎被认为在人类中是由免疫介导的,我们使用小鼠模型来研究T细胞和辅助性T细胞细胞因子在这些眼部病变免疫发病机制中的作用。皮下免疫并在基质内注射可溶性盘尾丝虫抗原(OvAg)的BALB/c小鼠出现了明显的角膜混浊和血管生成。角膜基质水肿,含有大量嗜酸性粒细胞和单核细胞。基于以下观察结果,免疫小鼠的基质性角膜炎被确定为T细胞依赖性:(a)免疫并在基质内注射OvAg的T细胞缺陷型裸鼠未出现角膜病变;(b)在基质内注射OvAg之前,将来自OvAg免疫的BALB/c小鼠的脾细胞过继转移到未免疫的裸鼠中会导致角膜炎的发生。OvAg刺激的淋巴结和脾细胞细胞因子产生依赖于CD4细胞,包括白细胞介素(IL)-4和IL-5,但不包括干扰素γ,表明主要是2型辅助性T细胞样反应。与干扰素γ相比,免疫的BALB/c小鼠和重建的裸鼠发炎角膜中的CD4和IL-4基因表达大大升高。IL-4基因被破坏的小鼠未发生角膜疾病,表明IL-4在盘尾丝虫介导的基质性角膜炎的免疫发病机制中至关重要。

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