How is Ocular Immune-Privilege Disrupted
Ocular immune-privilege (IP) is a reduced or altered immune response to an immunogen in the eye. It is believed that ocular IP is essential to prevent collateral damage from inflammatory responses and retain the clarity of the visual axis through the cornea and retina. IP is achieved through two mechanisms: unique anatomical structure and the immunosuppressive microenvironment of the eye. Anatomical structure that supports IP includes a limited lymphatic system, non-fenestrated endothelium with supportive cells such as pericytes, astrocytes, Müller cells and perivascular macrophages, and tight junctions formed by retinal pigment epithelial cells. The immunosuppressive microenvironment within the eye is created by soluble factors (e.g. α-MSH, TGF-β2) in the aqueous humour and membranous molecules (e.g. FasL, PD-L1, CD200) of cells in the intraocular compartment. In addition, tolerogenic Antigen Presenting Cells (APC) and homeostatic microbiome-induced regulatory T cells (Treg) also contribute to the immunosuppressive microenvironment. However, such IP is always threatened by physiological changes and pathological processes within the body. This short article will discuss common mechanisms which disrupt our ocular IP.