Li X Y, Niederkorn J Y
Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas 75235-9057, USA.
Ocul Immunol Inflamm. 1997 Dec;5(4):245-57. doi: 10.3109/09273949709085065.
Resistance to many pathogens, such as Listeria monocytogenes, is correlated with the host's capacity to generate a ThI cell-mediated immune response in which delayed-type hypersensitivity (DTH) is activated. A wide variety of antigens induce down-regulation of DTH when introduced into the anterior chamber of the eye. This immunoregulatory phenomenon has been termed anterior chamber-associated immune deviation (ACAID) and is believed to be a primary mechanism for the immune privilege of the anterior chamber. Suppression of DTH, as a result of anterior chamber priming, could carry significant risk to the host's well-being as the resistance to many pathogens relies heavily on DTH-dependent ThI responses. Studies were performed to determine if a bacterial pathogen, L. monocytogenes, introduced into the anterior chamber of the eye would induce a down-regulation of systemic DTH. Intracameral inoculation of infectious L. monocytogenes into genetically susceptible C3H and BALB/c mice did not induce suppression of DTH, but instead resulted in a significant footpad swelling response to bacterial antigens. Likewise, intracameral inoculation of L. monocytogenes into genetically resistant C57BL/6 mice also induced vibrant bacterial-specific DTH. Using an in-vitro model of ACAID, we showed that macrophage suspensions that were simultaneously exposed to L. monocytogenes and bovine serum albumin (BSA) antigens, in the presence of aqueous humor (AH), induced listerial-specific DTH responses, yet simultaneously induced suppression of BSA-specific DTH. Collectively, the results indicate that immune privilege is not extended to all foreign antigens that enter the anterior chamber of the eye, and as a result, some intraocular antigens can provoke strong systemic DTH. However, non-ACAID-inducing antigens do not prejudice the down-regulation of DTH by other antigens which normally induce ACAID.
对许多病原体（如单核细胞增生李斯特菌）的抵抗力与宿主产生Th1细胞介导的免疫反应的能力相关，在这种免疫反应中，迟发型超敏反应（DTH）被激活。当多种抗原被引入眼的前房时，会诱导DTH下调。这种免疫调节现象被称为前房相关免疫偏离（ACAID），被认为是前房免疫赦免的主要机制。由于前房致敏导致的DTH抑制可能会给宿主的健康带来重大风险，因为对许多病原体的抵抗力严重依赖于DTH依赖的Th1反应。进行了多项研究，以确定引入眼内前房的细菌病原体——单核细胞增生李斯特菌是否会诱导全身DTH下调。将感染性单核细胞增生李斯特菌眼内接种到基因易感的C3H和BALB/c小鼠中，并未诱导DTH抑制，反而导致对细菌抗原的显著足垫肿胀反应。同样，将单核细胞增生李斯特菌眼内接种到基因抗性的C57BL/6小鼠中也诱导了强烈的细菌特异性DTH。使用ACAID的体外模型，我们发现巨噬细胞悬液在房水（AH）存在的情况下，同时暴露于单核细胞增生李斯特菌和牛血清白蛋白（BSA）抗原，会诱导李斯特菌特异性DTH反应，但同时会诱导BSA特异性DTH抑制。总体而言，结果表明免疫赦免并不适用于所有进入眼内前房的外来抗原，因此，一些眼内抗原可引发强烈的全身DTH。然而，不诱导ACAID的抗原不会影响通常诱导ACAID的其他抗原对DTH的下调作用。
