Streilein J W, Okamoto S, Sano Y, Taylor A W
Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts 02114, USA.
Ann N Y Acad Sci. 2000;917:297-306. doi: 10.1111/j.1749-6632.2000.tb05396.x.
Ocular immune privilege arises from interactions between the immune apparatus and the eye itself, thereby providing immune protection for the eye that is devoid of sight-threatening inflammation. On the one hand, antigens injected intraocularly elicit deviant systemic immune responses that are devoid of immunogenic inflammation (Anterior Chamber-Associated Immune Deviation, ACAID). On the other hand, the ocular microenvironment (aqueous humor, secreted by cells that surround this chamber) suppresses intraocular expression of immunogenic inflammation. Several lines of evidence indicate that ocular immune privilege is under neural control. First, aqueous humor contains neuropeptides (alpha-MSH, VIP, CGRP) that inhibit and alter the functional properties of T lymphocytes and macrophages. Second, when corneal nerves are severed, the tissues surrounding the anterior chamber cease secreting immunosuppressive factors and ACAID fails--until the nerves regrow. Third, light deprivation abolishes the capacity of the anterior chamber to support ACAID induction, a process that is sensitive to neuropeptides and melatonin. The photoreceptor(s) responsible for ACAID are connected to the nervous system and may reside in the anterior segment and/or the retina. Thus, neural elements from the central nervous system and within the eye help to shape both the induction and the expression of ocular immunity, thereby promoting immune privilege.
眼免疫赦免源于免疫器官与眼睛自身之间的相互作用，从而为眼睛提供免疫保护，使其免受威胁视力的炎症影响。一方面，眼内注射的抗原引发异常的全身免疫反应，这种反应缺乏免疫原性炎症（前房相关免疫偏离，ACAID）。另一方面，眼微环境（房水，由围绕该腔室的细胞分泌）抑制眼内免疫原性炎症的表达。多条证据表明眼免疫赦免受神经控制。首先，房水中含有神经肽（α-促黑素、血管活性肠肽、降钙素基因相关肽），这些神经肽可抑制并改变T淋巴细胞和巨噬细胞的功能特性。其次，当切断角膜神经时，前房周围组织停止分泌免疫抑制因子，ACAID失效——直到神经重新生长。第三，剥夺光照会消除前房支持ACAID诱导的能力，这一过程对神经肽和褪黑素敏感。负责ACAID的光感受器与神经系统相连，可能位于眼前段和/或视网膜。因此，来自中枢神经系统和眼内的神经成分有助于塑造眼免疫的诱导和表达，从而促进免疫赦免。
