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

Small mechanical forces in immune cells measured at unprecedented sensitivity

Research

Oxford researchers have used advanced microscopy techniques to measure previously unseen forces generated by cells during an immune response; a breakthrough for mechanobiology and future advances in health and disease.

Oxford to collaborate with Janssen to map the cellular landscape of immune mediated disorders

Research

The University of Oxford has entered into a strategic collaboration with Janssen Biotech, Inc., one of the Janssen Pharmaceutical Companies of Johnson & Johnson.

Vascular loss shown to be the primary hallmark of aging

Research

New Research from the Kusumbe group at the Kennedy Institute of Rheumatology identifies vascular attrition, marked by pericyte to fibroblast differentiation, as a primary hallmark of aging and highlights organ-specific vascular changes with age.

Immunology preprint reviews launched in Nature Reviews Immunology

Research

The Oxford-Mount Sinai (OxMS) Preprint Journal Club has partnered with Nature Reviews Immunology to launch a monthly Preprint Watch column.

Drug may boost vaccine responses in older adults

General Research

A preliminary study shows that a drug which helps immune cells self-clean may improve vaccine protection in older adults

Living reviews launched by Oxford and Cardiff in the wake of COVID-19 research

Research

In a combined effort to help COVID-19 researchers the University of Oxford and Cardiff University have launched a series of “living reviews” in Oxford University Press’s new open access journal “Oxford Open Immunology”.