Researchers Discover Mitochondrial Protein as Target for Autoimmune Treatments

A study conducted by researchers at Swansea University has identified a mitochondrial protein that may serve as a promising target for treating autoimmune diseases. The research focuses on how this protein, known as ABHD11, regulates energy production in immune cells, particularly T-cells, which are often implicated in conditions like rheumatoid arthritis and type 1 diabetes.

T-cells play a vital role in the immune system by protecting the body from infections. However, in autoimmune diseases, these cells mistakenly attack the body’s own tissues. The study highlights that T-cells undergo metabolic changes when responding to infections, allowing them to process dietary fuels more effectively. In autoimmune disorders, these metabolic responses can become dysfunctional, leading to harmful effects on the body.

The findings, published in Nature Communications, indicate that inhibiting the ABHD11 protein can reduce the hyperactivity of T-cells. By using a drug to block the function of ABHD11, researchers observed a decrease in inflammation and a reduction in the production of inflammatory signals from T-cells. This approach has shown promise in delaying the onset of type 1 diabetes in experimental models.

Dr. Nick Jones, one of the lead researchers from Swansea University’s Medical School, emphasized the potential for new treatment options arising from this research. “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,” he said. Dr. Jones further noted that ABHD11 could be a valuable target for drugs aimed at reducing inflammation and preventing autoimmune flare-ups.

Current therapies for autoimmune diseases often come with significant side effects and do not work effectively for all patients. The study adds to the accumulating evidence that modifying immune cell metabolism can offer a safer and more effective approach to treatment.

The research team, which includes Professor Emma Vincent from the University of Bristol and Dr. James Pearson from Cardiff University, plans to explore the effects of blocking ABHD11 in various immune cell types. This could extend the therapeutic implications beyond just type 1 diabetes and rheumatoid arthritis to other autoimmune diseases.

Yasmin Jenkins, a joint first author and Ph.D. student at Swansea University, expressed enthusiasm about the findings. “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,” she stated. Jenkins added that further research could broaden the therapeutic benefits of targeting ABHD11 to a wider range of autoimmune conditions.

The implications of this research are significant. As the study progresses, it could pave the way for innovative treatments that improve the quality of life for individuals suffering from autoimmune diseases.

For more detailed information on this study, refer to the work of Benjamin J. Jenkins et al., titled “Mitochondrial ABHD11 inhibition drives sterol metabolism to modulate T-cell effector function,” published in Nature Communications in 2025 (DOI: 10.1038/s41467-025-65417-4).