ArticleNature communications2019
Innate lymphocyte-induced CXCR3B-mediated melanocyte apoptosis is a potential initiator of T-cell autoreactivity in vitiligo.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
93 citing papers in PubMed, 1 synthesis or guideline pooled it, 170 citations in OpenAlex.
- A meta-analysis of chemokines in vitiligo: Recruiting immune cells towards melanocytes.Frontiers in immunology · 2023Pooled it
- Apremilast and narrowband ultraviolet B combination therapy suppresses Th17 axis and promotes melanogenesis in vitiligo skin: a randomized, split-body, pilot study in skin types IV-VI.Archives of dermatological research · 2023Trial
- Oral gliadin-protected superoxide dismutase in addition to phototherapy for treating non-segmental vitiligo: A 24-week prospective randomized placebo-controlled study.Journal of the European Academy of Dermatology and Venereology : JEADV · 2021Trial
- Molecular Pathogenesis of Vitiligo: Emerging Roles of Epigenetic Regulation.Biomolecules & therapeutics · 2026Review
- Vitiligo as a Failure of Immune Resolution and Tissue Regeneration: From Stress Signals to Targeted Immune Modulation.Clinical reviews in allergy & immunology · 2026Review
- A Multifaceted Holistic Review of the Literature on Scar Dermatoses.International wound journal · 2026Review
- The immunology of vitiligo.Nature reviews. Immunology · 2026Review
- Mitochondrial DNA release via VDAC1 in keratinocytes: a key driver of innate immunity and vitiligo pathogenesis.Cell death & disease · 2026Article
- Pathogenesis of Vitiligo: Integrating Immune and Non-Immune Cell Crosstalk.The Journal of dermatology · 2026Review
- Oxidative stress in refractory and recurrent vitiligo: from immune amplification mechanisms to potential stratified antioxidant combination therapy.Frontiers in immunology · 2026Review
- Single-Cell Transcriptomics Reveals the Potential Role of GZMK+ CD8+ T Cells in Cell Senescence of Triple-Negative Breast Cancer.International journal of genomics · 2026Article
- Bidirectional Mendelian Randomization Suggests Causal Effects of 731 Immunophenotypes on Vitiligo Pathogenesis.Clinical, cosmetic and investigational dermatology · 2026Article
- Recent Advances in Vitiligo Treatment.ImmunoTargets and therapy · 2026Review
- The role of JAK3 and TEC family kinases in vitiligo pathogenesis.Frontiers in immunology · 2026Review
- Vitiligo.Nature reviews. Disease primers · 2025Review
- Emerging cell-based and cell-free therapeutic strategies for vitiligo.Journal of translational autoimmunity · 2025Review
- Cancer Risk in Vitiligo: No Evidence of Increased Prevalence-A Systematic Review and Meta-analysis.Dermatology and therapy · 2025Article
- A Scoping Review of Pathogenesis, Current Treatments, and Novel Approaches for Vitiligo.Journal of cosmetic dermatology · 2025Article
- Dysregulated Intracellular Signaling in the Pathogenesis of Vitiligo: An Update on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- Vitiligo.Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG · 2025Review
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-cells play a crucial role in progression of autoimmunity, including vitiligo, yet the initial steps triggering their activation and tissue damage remain unknown. Here we demonstrate increased presence of type-1 innate lymphoid cells (NK and ILC1)-producing interferon gamma (IFNγ) in the blood and in non-lesional skin of vitiligo patients. Melanocytes of vitiligo patients have strong basal expression of chemokine-receptor-3 (CXCR3) isoform B which is directly regulated by IFNγ. CXCR3B activation by CXCL10 at the surface of cultured human melanocytes induces their apoptosis. The remaining melanocytes, activated by the IFNγ production, express co-stimulatory markers which trigger T-cell proliferation and subsequent anti-melanocytic immunity. Inhibiting the CXCR3B activation prevents this apoptosis and the further activation of T cells. Our results emphasize the key role of CXCR3B in apoptosis of melanocytes and identify CXCR3B as a potential target to prevent and to treat vitiligo by acting at the early stages of melanocyte destruction.
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What OpenQuestion holds
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.