The eye is such that it needs to regulate both the immune and inflammation response in order to prevent visual impairment and blindness. Still, inflammation, infections and diseases occur. What mechanisms are in the eye that allow it to fight infection and is there a way to improve the immune response without damaging vision? Research at Thomas Jefferson University and Wayne State University studied these processes and this is what they found.
First comes inflammation and the eye. The eye needs to keep blood vessels away from the light pathway and restrict access of inflammatory cells that could cause damage. That leads to the question of how the eye manages inflammation. A study lead by Sue Menko, PhD at Thomas Jefferson University wanted to learn about the eye’s surveillance system and if it resolves inflammation.
Her lab found that macrophages (immune cells) with an immunoregulatory phenotype and regulatory T cells (specialized cells that maintain immune homeostasis and prevent disease) are recruited to the lens surface during inflammation. These cells restore balance and reduce inflammation. In addition, these cells stay on surface of the lens until the situation is resolved.
This study disproves the idea that the eye can’t care for itself and it leads to a greater understanding of how diseases like uveitis are resolved. This study also shows the importance of knowing the eye’s natural defenses. This knowledge could lead to better treatments for uveitis and other eye conditions. The next step in Dr. Menko’s research will focus on uncovering the means used by the eye to recruit immune cells to the lens and recognizing the alert system that led to inflammation.
When it comes to immunity and the eye, why do some eyes that shed the herpes simplex virus (HSV-1) on the eye surface not develop herpes stromal keratitis (HSK), whereas other infected eyes develop this disease? Susmit Suvas, PhD, Professor of Ophthalmology, Visual and Anatomical Sciences at Wayne State University wanted to find the answer to this question in order to develop new therapies to treat HSK, which is a major cause of infection-induced vision impairment in the U.S.
Two outcomes of HSV-1 are the development of herpes epithelial keratitis (HEK) and HSK. HEK is an eye infection that resolves on its own. HSK can cause vision loss. What is happening that leads to vision loss by way of HSK?
The research required the formation of memory T cells in HSV-1 infected corneas. What the study showed was the corneas that were infected with HSV-1 and didn’t develop HSK, had a large collection of protective tissue-resident memory T cells. The corneas that developed HSK had poor quantity and quality of tissue-resident memory T cells. The function of tissue-resident memory T cells is to eliminate the virus before it can do damage. Having enough high-quality tissue-resident memory T cells when someone has a cornea with HSV-1 can protect against the development of HSK.
When the immune cells don’t work properly and inflammation occurs, the eye can develop disease and possibly vision loss. Research projects at Thomas Jefferson University and Wayne State University demonstrate how these processes work to maintain vision and eye health and it may lead to treatments that improve outcomes for patient with uveitis, HSK or other eye diseases.
Sources:
https://pmc.ncbi.nlm.nih.gov/articles/PMC10418793/
https://pubmed.ncbi.nlm.nih.gov/39159867/
https://my.clevelandclinic.org/health/body/macrophages
https://my.clevelandclinic.org/health/body/23580-regulatory-t-cells