From bad to good: how anti-TNF therapy makes T-cells switch roles, from causing inflammation to reducing inflammation
Lead applicant - Professor Leonie Taams
Organisation - King's College London
Type of grant - Programme Grant Full application
Status of grant - Active
Amount of the original award - £1,185,431
Start date - 1 April 2016
Reference - 21139
What are the aims of this research?
The aim of this research is to investigate how anti-TNF therapy encourages certain immune cells, called inflammatory T-cells, to change roles from causing inflammation to reducing it.
Why is this research important?
Anti-TNF therapy has revolutionised the treatment of inflammatory arthritis. However, this type of therapy is expensive, not all patients respond to these drugs and it is still not possible to predict who these patients will be. Additionally, it remains unclear exactly how these drugs work inside the human body. An improved understanding of anti-TNF therapy is therefore required.
T-cells are a group of immune cells, some of which play a key role in causing the inflammation in seen in inflammatory arthritis. Previous research has showed that anti-TNF therapy triggers inflammatory T-cells to switch from being a cause of inflammation to stopping it. This happens because anti-TNF therapy promotes the T-cells to make a chemical called interleukin-10, which acts as a natural brake on the immune system, reducing inflammation. Identifying the molecules and processes that are responsible for triggering interleukin-10 production could reveal new therapeutic targets, and may help explain why certain patients do not respond to anti-TNF therapy.
How will the findings benefit patients?
Interleukin-10 is a naturally occurring within the body and therefore shows promise as a target for new treatments to control inflammation whilst avoiding side effects. This research hopes improve understanding of how anti-TNF drugs work, in particular how they promote interleukin-10 production. The outcomes from this research may lead to the development of new treatments, and may also explain why some patients do not respond to anti-TNF therapy.