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Hyperglycemia aggravates vitiligo through succinate/SUCNR1-mediated T cell activation
Pan Kang1, Yuqian Chang1, Tingting Wang1
1Department of Dermatology, Xijing Hospital, and.
The Journal of Clinical Investigation
|June 15, 2026
Summary
High blood sugar (hyperglycemia) worsens vitiligo by boosting CD8+ T cells via the succinate/SUCNR1 pathway. This research uncovers a key mechanism driving vitiligo progression and suggests SUCNR1 as a therapeutic target.
Area of Science:
- Immunology
- Dermatology
- Metabolomics
Background:
- Vitiligo is an autoimmune skin condition causing depigmentation, primarily driven by CD8+ T cells targeting melanocytes.
- The link between hyperglycemia and exacerbated autoimmune responses, including vitiligo, is recognized but lacks detailed mechanistic understanding.
Purpose of the Study:
- To investigate the immunometabolic mechanisms linking hyperglycemia to vitiligo.
- To identify specific metabolites involved in hyperglycemia-aggravated vitiligo progression.
Main Methods:
- A case-control study to correlate hyperglycemia and vitiligo.
- A mouse model to assess the impact of hyperglycemia on vitiligo.
- Targeted metabolomics to identify key metabolites.
Main Results:
- Hyperglycemia was correlated with vitiligo and aggravated the condition in a mouse model.
- Succinate was identified as a key metabolite mediating this effect.
- Succinate enhances CD8+ T cell activation via SUCNR1 and promotes skin-homing by influencing keratinocyte chemokine secretion through HIF-1α stabilization.
Conclusions:
- Hyperglycemia exacerbates vitiligo through the succinate/SUCNR1 axis, leading to CD8+ T cell hyperactivation.
- This pathway involves enhanced T cell activation and skin-homing.
- SUCNR1 presents a potential therapeutic target for managing hyperglycemia-associated vitiligo.
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