New Study Targets Mitochondrial Protein for Autoimmune Treatment

A recent study led by Swansea University has identified a promising approach to treat certain autoimmune diseases by targeting a mitochondrial protein that regulates energy production in immune cells. The research highlights a potential therapeutic pathway for conditions like rheumatoid arthritis and type 1 diabetes, which are characterized by the immune system mistakenly attacking the body’s own tissues.

Autoimmune diseases are primarily driven by T-cells, a type of immune cell essential for protecting the body from infections. In a healthy response, T-cells alter their metabolism—how they process dietary fuels such as sugar and protein—to effectively combat pathogens. However, in autoimmune conditions, these metabolic changes can become dysregulated, leading T-cells to cause harm instead of providing protection.

Discovering the Role of ABHD11

The study, published in Nature Communications, emphasizes the role of a protein called ABHD11, located in the mitochondria, which serve as the cell’s energy producers. Researchers found that inhibiting ABHD11 can reduce T-cell overactivity, thereby decreasing inflammation and the production of harmful inflammatory signals.

To reach this conclusion, the team analyzed immune cells from individuals both with and without type 1 diabetes and rheumatoid arthritis. They discovered that using a drug to block ABHD11 led to a significant reduction in inflammatory responses in T-cells. Notably, this inhibition also delayed the onset of type 1 diabetes in experimental models, suggesting a new avenue for therapeutic development.

Co-led by Dr. Nick Jones from Swansea University, along with Professor Emma Vincent from the University of Bristol and Dr. James Pearson from Cardiff University, the research underscores the need for alternative treatments in the field of autoimmune disorders. Current therapies often come with substantial side effects and may not be effective for all patients.

Future Directions and Potential Impact

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.” His comments reflect a growing consensus in the scientific community regarding the potential of metabolic modulation in immune responses.

Joint first author and Ph.D. student, Yasmin Jenkins, expressed optimism about the implications of their findings. She stated, “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.” Jenkins emphasized the importance of extending their research to examine the effects of ABHD11 inhibition in other immune cell types, which could broaden the range of autoimmune conditions that might benefit from this approach.

The research team plans to continue their investigation into the effects of targeting ABHD11, with the hope of expanding its therapeutic applications. As they explore the metabolic pathways of immune cells, the findings may lead to safer and more effective treatments for those suffering from autoimmune diseases.

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