Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

New research from Dr Richard Williams’ group at the Kennedy Institute suggests a route for the development of more selective – and effective – therapies for immune-mediated inflammatory disease.

Artists representation of T lymphoyctes. Signalling through TNFR2 receptor maintains Foxp3 expression in suppressor T lymphocytes.

Anti-TNF therapy is used to treat millions of patients worldwide for rheumatoid arthritis and other immune-mediated inflammatory diseases (IMIDs). Current anti-TNF therapies block both receptors for TNF - TNFR1 and TNFR2. However, new work from Dr Richard Williams’ lab suggests the development of therapies that specifically block TNFR1 could be advantageous for treating IMIDs.

The Williams lab found that TNFR2 plays a role in limiting the severity and duration of arthritis in animal models. Signalling through TNFR2 prevented methylation of the gene encoding Foxp3, a key protein for maintaining suppressor T regulatory cells that promote immune homeostasis.  

Richard said: “This research has been a great team effort and the results exemplify the complexities of cytokine biology. Thus, one molecule, TNF, can have completely opposing effects, depending on which receptor it acts upon.”

Although biologics targeting TNF have improved the lives of millions of people living with IMIDs, not all patients respond adequately to therapy. The new work suggests an approach to develop more selective therapies to increase efficacy and reduce side effects. 

Richard explains, “This research is likely to further stimulate the clinical development of novel biologics for IMIDs that specifically target TNFR1, whilst sparing TNFR2 signalling. In addition, the finding that TNFR2 controls the activity of regulatory T cells may have implications for cancer therapy as these cells are thought to contribute to immunosuppression within the tumour microenvironment.” 

The work was supported by funding from the Chang Gung Memorial Hospital and the Ministry of Science and Technology, Taiwan. 

Similar stories

Matthew Costa elected Fellow of Academy of Medical Sciences

Matthew Costa, Professor of Orthopaedic Trauma Surgery at NDORMS, has been elected a Fellow of the Academy of Medical Sciences.

COVID-19’s high blood clot risk

A recent study of patient health records found that around 1 in 100 people with COVID-19 had a venal or arterial thrombosis, with rates higher still among males, and particularly for those hospitalised.

REF 2021 results for medical research in Oxford

Today the UK Funding Bodies have published the outcomes of the recent national research assessment exercise, the Research Excellence Framework (REF) 2021.

Nurses' Day 2022

Today marks Nurses' Day 2022. This year's theme is #BestofNursing, so we chatted to some of our amazing Research Nurses about what the Best of Nursing means to them.

Rethinking pain management after injury

NDORMS researchers are to study whether a pain management treatment using cognitive behavioural therapy will improve recovery for people who have had a major leg injury.

Breakthrough in treatment for Dupuytren’s disease

Injection of the anti-TNF drug adalimumab into Dupuytren’s disease nodules is effective in reducing nodule hardness and nodule size.