New Study Identifies Protein Target for Autoimmune Disease Treatments

A groundbreaking study from Swansea University has identified a promising approach for treating autoimmune diseases by targeting a specific protein involved in energy regulation within immune cells. Autoimmune conditions, including rheumatoid arthritis and type 1 diabetes, arise when T-cells, which are typically tasked with defending the body against infections, mistakenly attack the body’s own tissues.

When T-cells respond to infections, they undergo significant metabolic changes to enable a robust immune response. In autoimmune diseases, these metabolic responses become dysregulated, leading to harmful effects on the body. The recent research, published in Nature Communications, focuses on a mitochondrial protein known as ABHD11, which plays a crucial role in controlling T-cell activity.

Key Findings from the Research

Researchers conducted their study on immune cells extracted from the blood of individuals both with and without type 1 diabetes and rheumatoid arthritis. They discovered that inhibiting the ABHD11 protein through a specific drug effectively reduced inflammation by curbing T-cell overactivity, thereby limiting the production of inflammatory signals.

Notably, the study also indicated that blocking ABHD11 delayed the onset of type 1 diabetes, suggesting a potential pathway for new therapeutic strategies aimed at managing autoimmune disorders. The research was co-led by Dr. Nick Jones from Swansea University, Professor Emma Vincent from the University of Bristol, and Dr. James Pearson from Cardiff University.

Dr. Jones remarked, “This research opens up exciting possibilities for developing new treatments that work by adjusting how immune cells use fuels from our diet—a process known as metabolism. ABHD11 could be a valuable target for drugs aimed at reducing inflammation and preventing autoimmune flare-ups.”

Future Implications and Research Directions

Current treatments for autoimmune diseases often come with significant side effects and do not work universally for all patients. This study contributes to the growing body of evidence that modifying immune cell metabolism may present a safer and more effective treatment option.

The research team plans to investigate the effects of inhibiting ABHD11 in different types of immune cells, which could have implications for a broader spectrum of autoimmune diseases. Yasmin Jenkins, the joint first author and Ph.D. student at Swansea University, expressed enthusiasm for future research, stating, “Manipulating immune cell metabolism in autoimmune disease offers a promising therapeutic avenue to explore, and our work highlights the exciting potential of ABHD11 as a target for the development of new treatments.”

As the team continues to explore the therapeutic benefits of targeting ABHD11, there is hope for advancing treatment options for a variety of autoimmune conditions.

To read more about this research, please refer to the publication by Benjamin J. Jenkins et al., titled “Mitochondrial ABHD11 inhibition drives sterol metabolism to modulate T-cell effector function,” in Nature Communications, 2025. DOI: 10.1038/s41467-025-65417-4.