A breakthrough from researchers from MIT and Massachusetts Eye and Ear has revealed that the body’s own immune cells may be the culprit behind the slow retinal deterioration associated with glaucoma.
The study found an unusually high number of T-cells present in the retinas of those suffering from the disease, suggesting the condition may have a previously undetected autoimmune cause.
Until now, scientists thought the primary cause of glaucoma was an increased pressure in the eye. This high eye pressure has been thought to result in a slow damage to the optic nerve, sometimes eventually leading to blindness. While measuring fluid pressure in the eye is still the best way to identify those at risk of developing glaucoma, it has not answered all the questions surrounding the disease.
People can be found to have the disease without any signs of elevated eye pressure, and conversely, some can have elevated eye pressure for years without any corresponding eye damage. Continued eye degradation has also been seen in many patients after eye pressure has been surgically reduced.
“That led us to the thought that this pressure change must be triggering something progressive, and the first thing that came to mind is that it has to be an immune response,” explains Dong Feng Chen, senior author on the new research.
The researchers initially examined the retinas of mice with induced high intraocular pressure. T-cells were unexpectedly found in the mouse retinas, which was strange as these immune cells are usually kept out of the retina by a strong layer of cells, often referred to as the blood-retina barrier. This suggested that something to do with the raising of eye pressure allowed these T-cells to slip past the eye’s protective barrier.
When eye pressure was raised in mice that had been engineered to lack T-cells only a minimal amount of damage was seen to be caused on the retina. This led the researchers to hypothesize that intraocular pressure in and of itself was not the primary cause of glaucoma eye damage.
The next stage of the research revealed that these T-cells found in the retina were specifically targeting heat shock proteins. It was suspected that these T-cells had been previously simulated by bacterial heat shock proteins, causing the immune cells to subsequently be primed to attack healthy eye cells in the presence of these organic proteins that normally should not attract T-cells.
The researchers discovered that glaucoma patients were found to have T-cells with heat shock protein sensitivity at levels five times higher than subjects without glaucoma. The overriding hypothesis is that it is these specific immune cells that cause the degenerative retina damage associated with glaucoma. It is still early days for the research and the next steps will involve further investigations into autoimmune processes that could lead to glaucoma.
The researchers suggest this mechanism could also be involved in other neurodegenerative diseases. A burgeoning field of research is suggesting autoimmune causes behind several neurological conditions, including Parkinson’s disease and psychosis. This new research hopes to pave the way for entirely new treatments targeting autoimmune activity as a way to combat a host of brain diseases.
“What we learn from the eye can be applied to the brain diseases, and may eventually help develop new methods of treatment and diagnosis,” says Dong Feng Chen, a senior author of the study.
The new research was published in the journal Nature Communications.