ANTERIOR CHAMBER INFLUENCE ON OCULAR ANTIGENS

对前房抗原的全身免疫反应是不同的 某些类型的免疫效应物(迟发型超敏反应和补体 固定抗体)被选择性地删除和/或抑制，而其他 效应物(细胞毒性T细胞、非补体结合抗体)有 诱导性。这种独特的免疫效应器模式被称为前部 小室相关免疫偏差(ACAID)。因为已经确定了 含有抗原的眼睛和脾的解剖完整性是 房室内注射后4-5天内诱导ACAID所需 抗原注射抗原，已经设计了实验来研究 这些要求的细胞和分子基础。两个相关的 假设将被实验检验：(1)定性和/或 不同数量的抗原特异性ACAID诱导信号逃逸到 从眼睛中注入抗原的血液；(2)在 脾，ACAID诱导信号优先激活TH2细胞，这是 进而损害TH1细胞的诱导，而TH1细胞负责 产生迟发性超敏反应和补体结合抗体。 最近的证据表明，眼睛内的免疫力表达可能 也是不正常的。需要检验的第三个假说是局部人工眼 因素(细胞和分子)作用于减少眼内的表达 迟发性超敏反应。由于诱导和表达的改变 存在对眼内抗原的免疫力，第四种假设是 异常免疫反应(ACAID)的测试状态可能对 对眼睛产生有害影响，导致免疫相关的眼部疾病。 为了检验这些假设，我们设计了四个具体目标： 1.研究眼睛作为ACAID诱导信号源的作用。 2.分析脾T细胞，鉴定和研究调节性淋巴细胞。 ACAID。 3.前房免疫效应细胞反应的特征 眼睛。 4.探讨ACAID与实验的可能关系 眼科疾病。 随着有关两国之间独特关系的新数据的积累 系统免疫系统和眼睛，我们的进步应该是可能的 了解眼部疾病的病因学，免疫系统 起着重要的致病作用。基于这样的认识， 然后可以设计策略来操纵特定的免疫系统 旨在预防和/或治疗免疫性眼病的方法。

Systemic immune responses to anterior chamber antigens are deviant in that certain types of immune effectors (delayed hypersensitivity and complement fixing antibodies) are selectively deleted and/or suppressed, whereas other effectors (cytotoxic T cells, non-complement fixing antibodies) are induced. This unique pattern of immune effectors has been termed Anterior Chamber Associate Immune Deviation (ACAID). Since it has been determined that anatomic integrity of he antigen-containing eye and the spleen is required for ACAID induction during the first 4-5 days after intracameral antigen injection of antigen, experiments have been designed to investigate the cellular and molecular bases of these requirements. Two related hypotheses will be tested experimentally: (1) A qualitatively and/or quantitatively distinct antigen-specific ACAID-inducing signal escapes into the blood from eyes into which antigen has been introduced; (2) In the spleen, the ACAID-inducing signal preferentially activates TH2 cells, which in turn impair the induction of TH1 cells that are responsible for the generation of delayed hypersensitivity and complement fixing antibodies. Recent evidence indicates that expression of immunity within the eye may also be abnormal. A third hypothesis to be tested is Local intraocular factors (cells and molecules) act to reduce intraocular expression of delayed hypersensitivity. Since alterations in induction and expression of immunity toward intraocular antigens exist, a fourth hypothesis to be tested states that Deviant immune responses (ACAID) may have beneficial or deleterious effect in the eye, leading to immune-related ocular disease. To test these hypotheses, we have devised four Specific Aims: 1. Study of the eye as a source of the ACAID-inducing signal. 2. Analyze splenic T cells to identify and study regulatory lymphocytes in ACAID. 3. Characterize immune effector cell responses in the anterior chamber of the eye. 4. Explore the possible relationships between ACAID and experimental ocular diseases. As new data accumulate concerning the unique relationship between the systemic immune system and the eye, progress should be possible in our understanding of the etiology of ocular disease in which the immune system plays an important pathogenic role. Based on this understanding, strategies can then be devised to manipulate the immune system in specific ways designed to prevent and/or treat immunopathogenic ocular diseases.