Project Update: Rheuma Tolerance for Cure (RTCure)

The Rheuma Tolerance for Cure (RTCure) project announced a breakthrough in its work on detection and prevention of Rheumatoid Arthritis (RA). 

An international team of scientists which includes researchers from the University of Glasgow, and is led by Dr. Andreas Ramming from the Chair of Internal Medicine III at University of Erlangen-Nuremberg  has  been able to decipher a molecular mechanism responsible for the ongoing activation of connective tissue cells.

The latest IMI newsletter outlined that the project team has identified a protein that plays a key role in the organ scarring that is a characteristic of many chronic diseases including idiopathic pulmonary fibrosis (lungs), cirrhosis (liver), kidney fibrosis, systemic sclerosis (the skin), and graft versus host disease (gut). 

In this latest study, researchers studied a protein called PU.1. In normal wound healing, the production of PU.1 is blocked, allowing the fibroblasts to return to a resting state. However, the researchers found that in people with diseases of the connective tissues, PU.1 is activated

This is key since Connective tissue cells called fibroblasts help to maintain the integrity of our organs and repair them when they are injured. Usually, once a wound has been healed, the fibroblasts dial down their activity and return to a resting state. However, in diseases such as those listed above, the fibroblasts are over-active, and produce excessive amounts of connective tissue. This results in organ scarring and impairs the ability of the organ to work correctly.

‘PU.1 binds to the DMA and re-programmes the connective tissue cells, resulting in a prolonged deposition of tissue components,’ explained Andreas Ramming of the Friedrich-Alexander-University Erlangen-Nürnberg in Germany, the lead researcher of the study.

The team emphasises that PU.1 is not the only factor involved in fibrosis. However, the new findings highlight the central role it plays in the process. Moreover, they showed that deactivating PU.1 causes the fibroblasts to return to their resting state. ‘PU.1 is like the conductor in an orchestra,’ said Dr Ramming. ‘If you take it out, the entire concert will collapse.’

The researchers conclude that drugs to block PU.1 could represent an effective approach to treating a wide range of fibrotic diseases.

You can find out more at the  project website 

You can also read more about the results in the nature journal of science (Link to Article)  and FAU website 

The RTCure project has received funding from the Innovative Medicines Initiative 2 Joint Undertaking under Grant Agreement no 777357. This joint undertaking receives support from the European Union's Horizon 2020 Research and Innovation Programme and EFPIA


Richard Buxbaum - Scotland Europa - NCP Services
Health, Well-being and Life Sciences