Li X Y, D'Orazio L T, Niederkorn J Y
Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas 75235-9057, USA.
Immunology. 1996 Sep;89(1):34-40. doi: 10.1046/j.1365-2567.1996.d01-714.x.
The immunological privilege of the anterior chamber (AC) of the eye is due, at least in part, to a selective antigen-specific down-regulation of delayed-type hypersensitivity (DTH) and a normal induction of antibody responses: a phenomenon that has been termed anterior chamber-associated immune deviation (ACAID). This dichotomy in the systemic immune responses is suggestive of a T-helper type-2 (Th2)-dominated immune phenotype in which a Th2 cell population is preferentially activated and cross-regulates T-helper type-1 (Th1) effector elements. This hypothesis was tested by comparing the cytokine pattern of antigen-pulsed spleen cells from mice primed in the anterior chamber with antigens that induce ACAID with responses in hosts primed with antigens that do not induce ACAID. The results indicated that CD4+ spleen cells from hosts primed in the AC with antigens that induce ACAID produced significant quantities of interleukin-10 (IL-10) but insignificant levels of IL-2, IL-4 and interferon-gamma (IFN-gamma). In contrast, hosts primed in the AC with antigens that do not induce ACAID, but instead elicit normal DTH, displayed cytokine patterns indicative of a Th1 response significant quantities of IL-2 and IFN-gamma were produced while IL-4 and IL-10 secretion was insignificantly different from normal controls. The immunological phenotype of the AC-primed hosts could be altered by systemic treatment with antibodies against either a Th1 cytokine (IFN-gamma) or a Th2 cytokine (IL-10). Hosts treated with anti-IL-10 antibody and subsequently primed in the AC with ACAID-inducing antigens developed normal DTH responses, while hosts treated with anti-IFN-gamma antibody and primed in the AC with antigens that normally produce positive DTH responses failed to develop positive DTH collectively the results support the proposition that immune privilege in the AC of the eye is due to the selective activation of a Th2 population that cross-regulates Th1 responses.
眼房水的免疫赦免至少部分归因于迟发型超敏反应（DTH）的选择性抗原特异性下调以及抗体反应的正常诱导：这种现象被称为房水相关免疫偏离（ACAID）。全身免疫反应中的这种二分法提示了一种以2型辅助性T细胞（Th2）为主导的免疫表型，其中Th2细胞群体被优先激活并对1型辅助性T细胞（Th1）效应元件进行交叉调节。通过比较在前房用诱导ACAID的抗原致敏的小鼠的抗原脉冲脾细胞的细胞因子模式与用不诱导ACAID的抗原致敏的宿主中的反应，对这一假设进行了检验。结果表明，在前房用诱导ACAID的抗原致敏的宿主的CD4 +脾细胞产生大量白细胞介素10（IL-10），但IL-2、IL-4和干扰素γ（IFN-γ）水平不显著。相比之下，在前房用不诱导ACAID但引发正常DTH的抗原致敏的宿主表现出指示Th1反应的细胞因子模式，产生大量IL-2和IFN-γ，而IL-4和IL-10的分泌与正常对照无显著差异。用针对Th1细胞因子（IFN-γ）或Th2细胞因子（IL-10）的抗体进行全身治疗可改变前房致敏宿主的免疫表型。用抗IL-10抗体治疗并随后在前房用诱导ACAID的抗原致敏的宿主产生正常的DTH反应，而用抗IFN-γ抗体治疗并在前房用通常产生阳性DTH反应的抗原致敏的宿主未能产生阳性DTH。总体而言，这些结果支持以下观点：眼房水的免疫赦免是由于Th2群体的选择性激活，该群体对Th1反应进行交叉调节。
