ArticleExperimental dermatology2022
NLRP3 inflammasome activation contributes to development of alopecia areata in C3H/HeJ mice.
Article in Experimental dermatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- The Role of Inflammasome in the Pathogenesis of Alopecia Areata: NLRP3 and Its Cascade Contribute to the Onset and Early Stage of Alopecia Areata.Annals of dermatology · 2026Article
- Early prediction of alopecia areata using machine learning modeling of neuro stress immune signatures from multi datasets.Scientific reports · 2025Article
- Fermented Yeast Complex Extract Promotes Hair Regrowth by Decreasing Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Article
- Pyroptosis in Alopecia Areata: Synthesizing Emerging Hypotheses and Charting a Path to New Therapies.Biomedicines · 2025Review
- Total glucosides of paeony inhibit NLRP3/caspase-1/GSDMD-mediated inflammation and pyroptosis in C3H/HeJ mice with alopecia areata.Biomolecules & biomedicine · 2025Article
- From mechanisms to therapies: current advances breakthroughs in alopecia areata immunopathology.Frontiers in immunology · 2025Review
- Novel potential therapeutic targets of alopecia areata.Frontiers in immunology · 2023Review
- NLRP3 inflammasome activation contributes to development of alopecia areata in C3H/HeJ mice.Experimental dermatology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alopecia areata (AA) is an autoimmune non-scarring hair loss disease. Recently, several reports have suggested that innate immune systems such as interferon-α (IFN-α)-producing plasmacytoid dendritic cells and NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasomes play a role in the pathogenesis of AA. However, critical studies about their involvement in the initiation of AA have not yet been reported. Therefore, we investigated the expression of innate immune cytokines in serum and skin, and examined the effect of a selective NLRP3 inhibitor, MCC950, on AA in C3H/HeJ mice, induced by transferring cultured skin-draining lymph node cells. IFN-α production was upregulated in lesions of AA-affected mice, and interleukin-1β in serum and skin was highly expressed before onset as well as postonset. Furthermore, MCC950 treatment prevented AA development and promoted hair growth in AA mouse models by reducing NLRP3 signalling and Th1/Tc1 chemokines and cytokines in the skin. These results suggest that NLRP3 inflammasome contributes to AA onset and chronicity, and NLRP3 inhibitor may be a potential therapeutic agent for AA.
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