Immune mechanisms of intraocular inflammation

Abstract

Understanding immune mechanisms of noninfectious intraocular inflammation via animal models, and the relatively more restricted insights that can be achieved through studies in humans, continues to generate successful immunotherapies. This translational conduit elaborates immunopathogenic mechanisms, and illuminates further prospects of tailored therapies and biomarkers of disease activity and prognosis. More recently, our increased understanding has moved on from the success of previous biologic therapies, such as anti-TNF and IFN-α treatments, revealing other possible avenues to target; for example, Th17 cells, immune cell migration and the use of T-regulatory and dendritic cells to induce immunological tolerance. We now recognize that the ocular environment is endowed with many regulatory mechanisms but is hardly privileged in as much as ocular inflammation remains prevalent. Nevertheless, future therapeutic and diagnostic developments will harness our understanding of the local immunoregulatory networks to not only restrain immune-mediated damage, but also to restore homeostasis and neuronal function. This article attempts to crystallize our understanding of local immune regulation and immune mechanisms leading to intraocular inflammation.

Keywords::

• autoimmune
• autoinflammation
• experimental autoimmune uveoretinitis
• intraocular inflammation
• macrophage
• T cell
• uveitis

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.