Study Reveals Mitochondrial Protein as Target for Autoimmune Treatment

A groundbreaking study conducted by researchers at Swansea University has identified a mitochondrial protein as a potential target for treating autoimmune diseases. The findings present a novel approach to managing conditions like rheumatoid arthritis and type 1 diabetes, which are characterized by an overactive immune response where T-cells erroneously attack the body’s own tissues.

Autoimmune diseases involve T-cells, which are crucial for defending against infections. In healthy individuals, these cells adjust their metabolism—how they process sugars and proteins—to effectively respond to pathogens. However, in autoimmune disorders, this metabolic adjustment goes awry, leading to tissue damage. The new research, published in Nature Communications, focuses on a protein known as ABHD11, which plays a significant role in regulating T-cell activity.

Researchers analyzed immune cells from the blood of individuals both with and without autoimmune conditions. They discovered that inhibiting ABHD11 with a specific drug effectively decreased inflammation by curbing T-cell overactivity. This intervention also delayed the onset of type 1 diabetes in experimental models, indicating the protein’s potential as a therapeutic target.

Dr. Nick Jones from Swansea University’s Medical School emphasized the significance of the 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. ABHD11 could be a valuable target for drugs aimed at reducing inflammation and preventing autoimmune flare-ups.”

The current treatments for autoimmune diseases often come with considerable side effects and may not be effective for all patients. The findings from this study suggest that altering immune cell metabolism could provide a safer, more effective alternative.

Joint first author Yasmin Jenkins, a Ph.D. student at Swansea University, expressed optimism about the implications of their research: “Manipulating immune cell metabolism in autoimmune disease offers a promising therapeutic avenue to explore, highlighting the exciting potential of ABHD11 as a target for new treatments.”

The research team also plans to investigate the effects of ABHD11 inhibition in other types of immune cells, broadening the scope of potential therapies for various autoimmune conditions. With further study, the hope is to develop treatments that can benefit a wider patient population.

Overall, this research marks an important step forward in understanding the metabolic processes involved in autoimmune diseases and presents a promising new target for therapeutic intervention.

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