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In a world first, researchers at the Kennedy Institute, Oxford have mapped the cellular dynamics following treatment with the most commonly used advanced therapy in autoimmune diseases. They have discovered why some patients benefit from this therapy while others do not, potentially paving the way for new therapies.

Man with inflammatory bowel disease holding his stomach © Shutterstock

Autoimmune diseases such as inflammatory bowel diseases (IBD), which include Crohn’s disease and ulcerative colitis, affect five percent of the global population. A major problem faced by the IBD community is that current drugs do not work for every patient. Given that it is not known why these drugs don’t work, the development of new treatments has been hindered.

A new approach by researchers at the Kennedy Institute of Rheumatology puts patients at the centre of the research question. The findings of the research, which was supported by the National Institute for Health and Care Research (NIHR) Oxford Biomedical Research Centre (BRC), NIHR Birmingham BRC and the Kennedy Trust for Rheumatology Research funding for A-TAP,  was published in Nature Immunology.

The interdisciplinary research team also included scientists and clinicians from Oxford’s Translational Gastroenterology and Liver Unit, the University of Birmingham and academic and industry colleagues from Australia and the United States.

The researchers followed patients before and after treatment with the most commonly used advanced therapy for IBD, anti-tumour necrosis factor (anti-TNF). The beneficial effect of anti-TNF in autoimmune diseases was first discovered at the Kennedy Institute of Rheumatology in the 1990s and revolutionised patient care. However, this treatment does not work in four out of ten patients.

For the first time, clinicians and scientists used a technology called ‘single-cell RNA-sequencing’ to characterise gut samples collected before and after anti-TNF treatment, one cell at a time – creating the largest cell atlas of IBD to date. They discovered the cellular basis for why some patients benefit from anti-TNF whilst others do not.

 

Read the full story on the The Kennedy Institute of Rheumatology website.