Oxford researchers have discovered why some patients benefit from the most commonly used advanced therapy for autoimmune diseases and some do not.

Autoimmune diseases, including inflammatory bowel diseases such as Crohn's disease and ulcerative colitis, affect five per cent of the global population.

A major issue for those with these types of diseases is the current drugs do not work for every patient.

The development of new treatments has been hindered by a lack of understanding of why these drugs do not work.

In a world first, the team at the University of Oxford mapped the cellular dynamics following anti-tumour necrosis factor (anti-TNF) treatment, potentially paving the way for new therapies.

The team from the university's Kennedy Institute of Rheumatology put patients at the centre of the research question, following them before and after they received the treatment.

For the first time, the team used a technology called single-cell RNA-sequencing to characterise gut samples collected before and after anti-TNF treatment, one cell at a time.

This created the largest cell atlas of inflammatory bowel diseases to date, revealing the cellular basis for why some patients benefit from anti-TNF while others do not.

Dr Tom Thomas, the first author of the paper, said: "Thus far, single-cell RNA-sequencing has generally been used to study inflammatory bowel diseases, a dynamic chronic disease, at a single time point.

"We embedded this technology in the patient journey to investigate a critical translational question and learn directly from the patient."

The study found epithelial and myeloid cells were key in determining the success of treatment.

Epithelial cells line the surface of the gut, and certain epithelial cells, known as goblet cells, produce gel-like mucin to protect the body from gut bacteria.

The team discovered patients who benefitted from anti-TNF had more goblet cells, and these exhibited higher levels of mucin expression.

Professor Calliope Dendrou, bioinformatics lead and co-senior author, said: "Conversations about anti-TNF outcome in inflammatory bowel diseases have been historically centred around non-response.

"We are shifting the paradigm by demonstrating that treatment benefit is determined by the balance between factors that drive remission versus inflammation."

Professor Christopher Buckley, co-senior author and director of clinical research at the Kennedy Institute of Rheumatology, added: “Understanding the cellular basis for treatment failure will act as a navigational aid for drug developers in designing the next generation of therapeutic agents, and will help clinicians to best position existing therapies.

"This first ‘longitudinal’ therapeutic atlas provides a foundational resource for scientists to compare against other treatments and across the many other autoimmune diseases.”