THE EFFECT OF LIGHT ON THE OCULAR IMMUNE RESPONSE

描述（改编自申请人摘要）：前房 是一个独特的微环境， 过程，特别是炎症反应，要么受损， 完全抑制。对延迟型的深刻抑制 对引入前房的抗原的超敏反应（DTH） 被称为前房相关免疫偏离（ACAID）， 被认为是维持免疫豁免的主要机制 在眼睛里。本申请将研究一种好奇的 在黑暗中饲养或适应的老鼠不能发展的现象 ACAID，而是对引入的抗原产生阳性DTH反应 进入前房目前的假设是， 剥夺刺激眼内白细胞介素-1的产生 IL-1和/或P物质（SP），其反过来激活T细胞， 前房最终的结果是激活，而不是下降- 抗原特异性免疫的调节。四个具体目标将是 根据这一假设。它们是：（1）确定 抗IL-1 α抗体逆转暗饲养的机制 （2）探讨神经肽在诱导和抑制细胞凋亡中的作用。 （3）探讨炎性细胞的功能， 在黑暗中前房接种抗原后积累- （4）探讨光、暗对光适应小鼠的影响 暴露对常驻眼细胞和免疫效应机制的影响 the eye.本项目的长期目标是更好地了解 ACAID和免疫赦免的分子基础。

DESCRIPTION (Adapted from applicant's abstract): The anterior chamber of the eye is a unique microenvironment in which immunological processes, especially inflammatory responses, are either impaired or totally inhibited. The profound suppression of delayed-type hypersensitivity (DTH) to antigens introduced into the anterior chamber has been termed anterior chamber-associated immune deviation (ACAID) and is believed to be the primary mechanism for sustaining immune privilege within the eye. The present application will examine a curious phenomenon in which mice reared or adapted to the dark cannot develop ACAID and instead, develop positive DTH responses to antigens introduced into the anterior chamber. The working hypothesis is that light deprivation stimulates the intraocular production of interleukin-1 (IL-1) and/or substance P (SP) which in turn activates T cells in the anterior chamber. The net result is activation, rather than down- regulation, of antigen-specific immunity. Four specific aims will be addressed pursuant to this hypothesis. They are: (1) determine the mechanisms by which anti-IL-1 alpha antibody reverses the dark-rearing effect; (2) explore the role of neuropeptides in both the induction and abolition of ACAID; (3) explore the function of inflammatory cells that accumulate following anterior chamber inoculation of antigen in dark- and light-adapted mice; and (4) explore the effect of light and dark exposure on the resident ocular cells and immune effector mechanisms in the eye. The long range goal of this project is to better understand the molecular basis of ACAID and immune privilege.