New study identifies mitochondrial protein as key target in autoimmune disease treatment

New study identifies mitochondrial protein as key target in autoimmune disease treatment
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Professor Dame Jean Thomas Chancellor | Swansea University

A recent study published in Nature Communications has identified a new potential target for treating autoimmune diseases, such as rheumatoid arthritis and type 1 diabetes. The research focuses on T-cells, immune cells that normally protect the body from infections but can mistakenly attack healthy tissues in autoimmune conditions.

The study found that a protein called ABHD11, located in the mitochondria of cells, plays an important role in controlling T-cell activity. Researchers examined immune cells from people with and without type 1 diabetes or rheumatoid arthritis. They discovered that using a drug to block ABHD11 reduced inflammation by limiting the overactivity of T-cells and their production of inflammatory signals.

Blocking ABHD11 not only decreased inflammation but also delayed the onset of type 1 diabetes in experimental models. This suggests that targeting this protein could lead to new therapies for managing autoimmune diseases.

Dr Nick Jones from Swansea University’s Medical School commented: “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.”

He added: “Current treatments for autoimmune diseases can have significant side effects and don’t work for everyone. This study adds to growing evidence that adjusting immune cell metabolism could offer a safer and more effective approach.”

The research was co-led by Dr Nick Jones (Swansea University), Professor Emma Vincent (University of Bristol), and Dr James Pearson (Cardiff University). The team plans to investigate whether blocking ABHD11 affects other types of immune cells, which may have implications for additional autoimmune disorders.

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