Systemic immune response to Acanthamoeba keratitis in the Chinese hamster.
Systemic immune response to Acanthamoeba keratitis in the Chinese hamster.
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DOI：
10.3109/09273949709085064
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发表时间：
1997-12
影响因子：
3.3
通讯作者：
F. van Klink;H. Leher;M. Jager;H. Alizadeh;W. Taylor;J. Niederkorn
中科院分区：
文献类型：
--
作者：
F. van Klink;H. Leher;M. Jager;H. Alizadeh;W. Taylor;J. Niederkorn
复发是阿米巴角膜炎的一个常见和令人不安的特征，表明角膜感染这种生物体不能刺激全身免疫装置。本文研究了中国仓鼠对阿米巴角膜炎的细胞免疫和体液免疫应答。角膜感染A. castellanii未能诱导迟发型超敏反应（DTH）或血清IgG抗体对寄生虫抗原。未能诱导细胞介导和体液免疫并不导致无反应性或耐受性，因为随后的肌内（i.m.）用寄生虫抗原免疫引起强烈的DTH和IgG抗体应答。角膜感染不能诱导初级细胞介导的免疫应答是由于角膜中央缺乏常驻抗原呈递细胞，因为在阿米巴感染前诱导朗格汉斯细胞（LC）迁移到角膜中央促进了寄生虫特异性DTH的发展。虽然存在的居民LC并没有促进发展的主要体液免疫反应，随后的i.m.免疫引起寄生虫特异性IgG抗体产生的增加，这是回忆应答的指示。总的来说，结果表明，在没有常驻抗原呈递细胞的情况下，角膜感染阿米巴未能刺激原代细胞介导的或体液免疫。外周LC诱导进入中央角膜上皮可促进寄生虫特异性DTH的发生，但不会加剧角膜疾病。
Recrudescence is a common and troubling feature of Acanthamoeba keratitis and suggests that corneal infection with this organism fails to stimulate the systemic immune apparatus. The present study examined the cell-mediated and humoral immune responses to Acanthamoeba keratitis in the Chinese hamster. Corneal infection with A. castellanii failed to induce either delayed-type hypersensitivity (DTH) or serum IgG antibody against parasite antigens. The failure to induce cell-mediated and humoral immunity did not result in anergy or tolerance since subsequent intramuscular (i.m.) immunization with parasite antigens elicited robust DTH and IgG antibody responses. The inability of corneal infections to induce primary cell-mediated immune responses was due to the absence of resident antigen-presenting cells in the central cornea because induction of Langerhans cell (LC) migration into the central cornea prior to infection with Acanthamoeba promoted the development of parasite-specific DTH. Although the presence of resident LC did not promote the development of a primary humoral immune response, subsequent i.m. immunization elicited heightened parasite-specific IgG antibody production which was indicative of an anamnestic response. Collectively, the results indicate that in the absence of resident antigen-presenting cells, corneal infection with Acanthamoeba fails to stimulate primary cell-mediated or humoral immunity. Induction of peripheral LC into the central corneal epithelium promotes the development of parasite-specific DTH, but does not exacerbate corneal disease.