ArticleThe Journal of investigative dermatology2012
Vitiligo-inducing phenols activate the unfolded protein response in melanocytes resulting in upregulation of IL6 and IL8.
Article in The Journal of investigative dermatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
75 citing papers in PubMed, 190 citations in OpenAlex.
- Design and construction of cuttlefish ink derived melanin complexed microneedles for microenvironment regulation to improve vitiligo treatment.Marine life science & technology · 2026Article
- Chemotherapy-Induced Alopecia Beyond Cytotoxicity: Hair Follicle Immune Privilege Collapse and JAK-STAT Signaling.International journal of molecular sciences · 2026Review
- Review
- The immunology of vitiligo.Nature reviews. Immunology · 2026Review
- In Vitro Safety Profiling and Leukoderma-Relevant Hazard Assessment of Raspberry Ketone VersusMolecules (Basel, Switzerland) · 2026Article
- Oxidative stress in refractory and recurrent vitiligo: from immune amplification mechanisms to potential stratified antioxidant combination therapy.Frontiers in immunology · 2026Review
- Dysregulated Intracellular Signaling in the Pathogenesis of Vitiligo: An Update on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- Deciphering Depigmentation: Mouse Models for Vitiligo Research.The Journal of investigative dermatology · 2025Review
- The immunological pathogenesis of vitiligo and the potential role of mesenchymal stromal/stem cells in its treatment.Journal of translational medicine · 2025Review
- Glutamate promotes triple-negative breast cancer development through IRE1α/XBP1-mediated macrophage polarization: mechanism insights and therapy.Discover oncology · 2025Article
- Role of oxeiptosis in disease mechanisms and therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2025Review
- Implication of Immunobiological Function of Melanocytes in Dermatology.Clinical reviews in allergy & immunology · 2025Review
- Repigmentation by body region in patients with vitiligo treated with ruxolitinib cream over 52 weeks.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Article
- Recent clinical and mechanistic insights into vitiligo offer new treatment options for cell-specific autoimmunity.The Journal of clinical investigation · 2025Review
- Innate immune activation in vitiligo: mechanisms and pathophysiological implications.Frontiers in immunology · 2025Review
- Candidate approaches for predicting vitiligo recurrence: an effective model and biomarkers.Frontiers in immunology · 2025Article
- Case Report: Treating one autoimmune disease induces another: the paradox of TNF-alpha inhibitor therapies.Frontiers in immunology · 2025Article
- Enhancing antitumor immunity: the role of immune checkpoint inhibitors, anti-angiogenic therapy, and macrophage reprogramming.Frontiers in oncology · 2025Review
- Endoplasmic Reticulum Dysfunction: An Emerging Mechanism of Vitiligo Pathogenesis.Clinical, cosmetic and investigational dermatology · 2024Review
- The emerging role of effector functions exerted by tissue-resident memory T cells.Oxford open immunology · 2024Review
15 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Vitiligo is characterized by depigmented skin patches caused by loss of epidermal melanocytes. Oxidative stress may have a role in vitiligo onset, while autoimmunity contributes to disease progression. In this study, we sought to identify mechanisms that link disease triggers and spreading of lesions. A hallmark of melanocytes at the periphery of vitiligo lesions is dilation of the endoplasmic reticulum (ER). We hypothesized that oxidative stress results in redox disruptions that extend to the ER, causing accumulation of misfolded peptides, which activates the unfolded protein response (UPR). We used 4-tertiary butyl phenol and monobenzyl ether of hydroquinone, known triggers of vitiligo. We show that expression of key UPR components, including the transcription factor X-box-binding protein 1 (XBP1), is increased following exposure of melanocytes to phenols. XBP1 activation increases production of immune mediators IL6 and IL8. Co-treatment with XBP1 inhibitors reduced IL6 and IL8 production induced by phenols, while overexpression of XBP1 alone increased their expression. Thus, melanocytes themselves produce cytokines associated with activation of an immune response following exposure to chemical triggers of vitiligo. These results expand our understanding of the mechanisms underlying melanocyte loss in vitiligo and pathways linking environmental stressors and autoimmunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.