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NLRP3 autophagic degradation disruption in melanocytes contributes to vitiligo development

Cell Death & Differentiation (2025)Cite this article

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Abstract

NLRP3 functions as a critical intracellular danger sensor for inflammasome activation, playing a crucial role in autoimmune diseases. Vitiligo progression has been linked to NLRP3, yet its specific involvement in melanocytes of vitiligo remains poorly understood. In this study, we demonstrate that NLRP3 expression is significantly upregulated in the melanocytes of vitiligo patients and melanoma-Treg-induced vitiligo mouse model. Genetic knockout of NLRP3 effectively alleviates vitiligo progression in these mice. Our mechanistic investigations reveal that the downregulation of the E3 ligase β-TrCP1 in vitiligo melanocytes decreases K27-linked ubiquitination levels of NLRP3, which in turn weakens its interaction with the autophagy receptor NDP52. This disruption impairs the selective autophagic degradation of NLRP3, leading to hyperactivation of inflammation and pyroptosis in melanocytes, thereby accelerating vitiligo pathogenesis. Notably, melanocyte-specific knockdown of NLRP3 using lysine-proline-valine (KPV)-modified deformable liposomes (KPV-Lipos) carrying Nlrp3 shRNA significantly alleviates vitiligo development. This study elucidates the mechanism by which autophagy dysfunction mediated excessive NLRP3 inflammasome activation in melanocytes contributes to vitiligo pathogenesis, highlighting potential therapeutic strategies targeting these pathways for the treatment of vitiligo and other pigment-related skin diseases.

Overview of disrupted NLRP3 autophagic degradation in vitiligo melanocytes. In healthy melanocytes, NLRP3 expression is upregulated when subjected to oxidative stress, along with an increase in the E3 ligase β-TrCP1, which enhances the K27-linked ubiquitination of NLRP3 and further strengthens its binding to the autophagy receptor protein NDP52, thus effectively suppressing the excessive inflammatory response. Whereas in the melanocytes of vitiligo patients, decreased expression of β-TrCP1 leads to downregulation of K27-linked ubiquitination in NLRP3, thus inhibiting its autophagic degradation. The persistent activation of NLRP3 in vitiligo melanocytes promotes the cleavage of pro-IL-1β and GSDMD. GSDMD-N subsequently forms pores on the cell membrane, which causes the release of IL-1β and results in melanocyte pyroptosis. In our study, we utilize KPV-Lipos with Nlrp3 shRNA to precisely knockdown NLRP3 expression in melanocytes and effectively alleviate vitiligo development, which provide a potentially promising strategy for the treatment of vitiligo. MC, melanocytes.

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Fig. 1: NLRP3 expression is enhanced as vitiligo progresses.
Fig. 2: The NLRP3 inflammasome exhibits high levels of expression and activation in PIG3V.
Fig. 3: Autophagic degradation of NLRP3 is impaired in PIG3V.
Fig. 4: Downregulation of β-TrCP1 results in impaired K27-linked ubiquitination of NLRP3 in PIG3V.
Fig. 5: KPV-Lipo carrying shNlrp3 specifically targets melanocytes.
Fig. 6: Melanocyte-specific knockdown of Nlrp3 alleviates vitiligo progression induced by B16F10.

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We declare that all the data and materials are available upon request.

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Acknowledgements

We thank Dr. Chunying Li (Xijing Hospital, Fourth Military Medical University) for providing PIG1 and PIG3V cells and Dr. Jun Cui (Sun Yat-sen University) for providing plasmids for p62, NDP52, Tollip and OPTN.

Funding

This work was supported by grants from the National Natural Science Foundation of China (82572009, 82473549, 82371761, and 82171741), National Key R&D Program of China (2024YFC2309700), Guangdong Basic and Applied Basic Research Foundation (2023A1515010421), Science and Technology Program of Guangzhou (2025A04J7166), Zhejiang Provincial Natural Science Foundation of China (LY23H110001), and The Hangzhou Medical Key Discipline Construction Project ([2025]36-7).

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  1. These authors contributed equally: Ke Zeng, Yuqi Zhu, Zhongxin Han.

Authors and Affiliations

  1. Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China

    Ke Zeng, Zhongxin Han, Siyi Xiong, Zilong Xiao, Yingchao Xie, Weiwei Liu & Xiao Yu

  2. Department of Dermatology, Hangzhou Third Hospital affiliated to Zhejiang Chinese Medical University, Hangzhou, China

    Yuqi Zhu, Shiyu Jin & Tingru Dong

  3. Department of Dermatology, Traditional Chinese and Western Medicine Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

    Yan Zhao

  4. Department of Pharmacy, Hangzhou Third Hospital affiliated to Zhejiang Chinese Medical University, Hangzhou, China

    Lan Lan

  5. Institute of Pharmaceutics, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China

    Yongzhong Du

  6. Department of Dermatology, Hangzhou Third People’s Hospital, Hangzhou, China

    Cuiping Guan & Xiuzu Song

  7. Department of Clinical Laboratory Medicine, Guangdong Provincial People’s Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China

    Xiao Yu

  8. Guangdong Provincial Key Laboratory of Single-cell and Extracellular Vesicles, Southern Medical University, Guangzhou, China

    Xiao Yu

  9. State Key Laboratory of Multi-organ Injury Prevention and Treatment, Southern Medical University, Guangzhou, China

    Xiao Yu

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Contributions

Ke Zeng, Yuqi Zhu and Zhongxin Han designed the study, performed the major experiments and analyzed data. Siyi Xiong, Yan Zhao, Zilong Xiao, Yingchao Xie, Weiwei Liu and Yongzhong Du provided technique support in some experiments. Ke Zeng, Yuqi Zhu and Zhongxin Han wrote the original manuscript. Xiao Yu and Cuiping Guan edited the manuscript. Shiyu Jin, Tingru Dong and Lan Lan performed some animal experiments. Xiao Yu, Cuiping Guan and Xiuzu Song supervised all experiments and verified the experimental data.

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Correspondence to Cuiping Guan, Xiao Yu or Xiuzu Song.

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All methods were performed in accordance with the relevant guidelines and regulations. Animal (mice) procedures were approved by Southern Medical University Animal Care and Use Committee (Protocol number: L2019043). Human tissue collection and subsequent studies were approved by the ethics committee of Hangzhou Third People’s Hospital, Hangzhou, China, and informed consent was obtained from all patients prior to participation. (Protocol number: 2022KA007).

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Zeng, K., Zhu, Y., Han, Z. et al. NLRP3 autophagic degradation disruption in melanocytes contributes to vitiligo development. Cell Death Differ (2025). https://doi.org/10.1038/s41418-025-01578-5

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