Abstract
Ocular function depends on a high level of anatomical integrity. This is threatened by inflammation, which alters the local tissue over short and long time-scales. Uveitis due to autoimmune disease, especially when it involves the retina, leads to persistent changes in how the eye interacts with the immune system. The normal pattern of immune surveillance, which for immune privileged tissues is limited, is re-programmed. Many cell types, that are not usually present in the eye, become detectable. There are changes in the tissue homeostasis and integrity. In both human disease and mouse models, in the most extreme cases, immunopathological findings consistent with development of ectopic lymphoid-like structures and disrupted angiogenesis accompany severely impaired eye function. Understanding how the ocular environment is shaped by persistent inflammation is crucial to developing novel approaches to treatment.
Highlights
The immune response addresses an enormous variety of challenges across many different time-scales from acute viral illness, cleared within a week, to chronic infections, like tuberculosis and herpes viruses, that can remain dormant for decades
Studies of experimental autoimmune uveitis (EAU) often focus on the acute phase of the response, but EAU has been described as monophasic, sensitive analyses of the disease in the mouse has demonstrated that while the tempo of inflammation it is less after the primary peak of inflammation it remains a dynamic process, the immune content and immunosurveillance of the tissue is radically altered by the disease (Kerr et al, 2008b) and subsequent studies have confirmed and extended this observation (Chen et al, 2012; Chu et al, 2013; Oh et al, 2011)
The exquisite specificity that can be achieved has been nicely demonstrated for CD8+ T cell killing, where within a skin graft composed of a mixture of Major histocompatibility complex (MHC) haplotypes, only those cells that elicit an allogeneic immune response are killed while non-allogenic neighbours survive (Rosenberg and Singer, 1988)
Summary
The immune response addresses an enormous variety of challenges across many different time-scales from acute viral illness, cleared within a week, to chronic infections, like tuberculosis and herpes viruses, that can remain dormant for decades. In addition to harm caused by acute inflammation, a previously healthy tissue may be compelled in the long term to submit to much more rigorous scrutiny than is customary Accommodating such change in tissues is a necessary requirement for immune memory. There is growing evidence that local tissue responses can play a critical role in defending an individual from reinfection at specific sites (Schenkel and Masopust, 2014; Steinert et al, 2015) It is clear from recent work in animal models and human disease, that the long-term local changes which occur are important. These effects manifest across a multiplicity of individual core functions including: immune tissue neogenesis, angiogenesis, stromal remodelling and the local expression of co-inhibitory molecules. Understanding the new patterns of immunosurveillance that are consequent upon autoimmune disease will be important for managing future immunotherapies
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