Brief plain language background
Auto-immune conditions involve the immune system (white blood cells or antibodies) targeting and damaging parts of the body. One example is Grave’s disease (GD), where the immune system produces antibodies causing the thyroid gland to produce too much thyroid hormone.
Some people with GD develop thyroid eye disease (TED) – damaging and inflaming fatty tissues behind they eye – which can be painful, disfiguring and lead to sight loss.
What problem/knowledge gap does it help address
It is unknown why some people with GD go onto developing TED. Current treatments are not effective, with some patients requiring surgery to relieve symptoms and preserve sight.
A recent new treatment called teprotumumab has shown promise in reversing TED by targeting a specific type of cell called fibroblasts. These are involved in signalling to other cell types in the fatty tissue behind the eye.
There may be additional targets in the eye’s fatty tissue that could help predict the risk of developing TED or treat the condition.
Aim of the project
To investigate additional fibroblast receptors as drivers of TED and identify which receptors are recognised by autoantibodies.
This project also aims to further the career progression of the applicant, as amongst other benefits, the findings could form the basis of future grant applications in TED.
Key procedures/objectives
- Identify the target of antibodies in the eye’s fatty tissue in GD.
- Examine the processes driven by autoantibodies binding with fibroblasts.
- Characterise the levels of cell signalling to fibroblasts in the eye that drive TED.
Potential impact on people with sight loss
The identification of additional targets that drive TED could lead to developments of potential treatments for the condition. As well as reducing TED symptoms, some targets may have potential to act as a “marker” for the condition, which means those at a greater risk of developing TED can be monitored more effectively.
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