A new study from Swansea University points to ABHD11 – a mitochondrial protein that helps control how T cells use fuel – as a promising target for autoimmune diseases like type 1 diabetes and rheumatoid arthritis. By blocking ABHD11, the researchers were able to “cool down” overactive T cells and delay disease in animal models.

In other words, this is immunometabolism in action: instead of only blocking inflammatory signals (like we do with JAK inhibitors), you gently rewire how immune cells produce energy so they become less aggressive.

Could this be useful in vitiligo? Conceptually, yes. Vitiligo is driven by long-lived, overactive T cells in the skin, and we already have proof from experimental work that changing their metabolism can calm the disease.

However, ABHD11 is also present in melanocytes – the pigment-making cells that vitiligo destroys – and the pathway it modulates (via cholesterol metabolites and LXR activation) is known to reduce pigment production. That is a red flag for a disease where restoring pigment is the main goal.

So for now, I would treat ABHD11 as an interesting research probe, not a near-term drug target for vitiligo. It’s a clever way to tune immune cells, but we need careful studies in vitiligo models to be sure we are not simultaneously undermining the very melanocytes we’re trying to protect.

 

— Yan Valle

Professor h.c., CEO VR Foundation | Author, A No-Nonsense Guide to Vitiligo

 

Suggested reading: 

• Defining the Landscape of Hand Vitiligo
• Rethinking Vitiligo – Five Distinct Faces of a Complex Disease
• Biologic Therapies for Vitiligo: A New Era of Hope

Listen to podcast Deep Dive In Vitiligo:

• Vitiligo Pipeline 2025: Winners, Watchlist, What’s Next (Ep. 41)
• Sixty Years Of Vitiligo Research — Where Are We Now and What Comes Next? (Ep. 35)

Our podcast Deep Dive In Vitiligo is available on all digital platforms, like Apple Podcasts, Spotify, Amazon, YouTube Music, Podcast Addict, iHeart and elsewhere.