ReviewBiomedicines2022
Current Concepts of Vitiligo Immunopathogenesis.
Review in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 3 of them syntheses 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
39 citing papers in PubMed, 3 syntheses or guidelines pooled it, 56 citations in OpenAlex.
- Regulatory T Cell Dysregulation in Vitiligo: A Meta-Analysis and Systematic Review of Immune Mechanisms and Therapeutic Perspectives.International journal of dermatology · 2025Pooled it
- Psychiatric Comorbidities and Quality-of-Life Burden in Pediatric Patients With Vitiligo: A Systematic Review and Meta-Analysis.Pediatric dermatology · 2025Pooled it
- Efficacy and Safety of Janus Kinase Inhibitors in Patients with Vitiligo: A Systematic Review and Meta-Analysis.Clinical pharmacology and therapeutics · 2025Pooled it
- Hair Follicle Stem Cells: Emerging Physiology and Therapeutic Applications.Stem cell reviews and reports · 2026Review
- The CREM-IL-15 axis: decoding the persistence-exhaustion paradox in NK cell immunotherapy.Cancer immunology, immunotherapy : CII · 2026Review
- Interleukin 32 Exacerbates Vitiligo by Promoting Inflammation and Oxidative Stress-induced Injury in Melanocytes.Inflammation · 2026Article
- Association of Serum Interleukin-17 Levels With Vitiligo: A Pilot Cross-Sectional Comparative Study.Cureus · 2026Article
- Vitiligo Information Resource database v3.NPJ systems biology and applications · 2026Article
- Review
- Bidirectional Mendelian Randomization Suggests Causal Effects of 731 Immunophenotypes on Vitiligo Pathogenesis.Clinical, cosmetic and investigational dermatology · 2026Article
- Review
- Circulating CLAJID innovations : skin science from molecules to population health · 2025Review
- Sirtuin1 Deficiency Could Exacerbate Melanocyte Apoptosis Under Endoplasmic Reticulum Stress.Inflammation · 2025Article
- Cullin-3 and Regulatory Biomolecules Profiling in Vitiligo: Integrated Docking, Clinical, and In Silico Insights.Biomolecules · 2025Article
- The immunological pathogenesis of vitiligo and the potential role of mesenchymal stromal/stem cells in its treatment.Journal of translational medicine · 2025Review
- Beyond skin deep: exploring the complex molecular mechanisms and holistic management strategies of vitiligo.Archives of dermatological research · 2025Review
- Efficacy of CLT4A variants as immunoregulatory molecules among Vitiligo patients in Saudi Arabia.Scientific reports · 2025Article
- Dietary Interventions, Supplements, and Plant-Derived Compounds for Adjunct Vitiligo Management: A Review of the Literature.Nutrients · 2025Review
- Commentary: Local sympathetic nerve depletion does not alter vitiligo progression in a mouse model.Frontiers in medicine · 2025Article
- Single-Cell Transcriptomic Analysis Reveals an Inflammatory Antigen-Presenting Macrophages Subtype Drive Vitiligo Pathogenesis Through STAT1-Mediated Dual Mechanisms.Mediators of inflammation · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Vitiligo is an acquired immune-mediated disorder of pigmentation clinically characterized by well-defined depigmented or chalk-white macules and patches on the skin. The prevalence of vitiligo varies by geographical area, affecting 0.5% to 2% of the population. The disease imposes a significant psychological burden due to its major impact on patients' social and emotional aspects of life. Given its autoimmune background, vitiligo is frequently associated with other autoimmune diseases or immune-mediated diseases. Vitiligo is a multifaceted disorder that involves both genetic predisposition and environmental triggers. In recent years, major predisposing genetic loci for the development of vitiligo have been discovered. The current findings emphasize the critical role of immune cells and their mediators in the immunopathogenesis of vitiligo. Oxidative-stress-mediated activation of innate immunity cells such as dendritic cells, natural killer, and ILC-1 cells is thought to be a key event in the early onset of vitiligo. Innate immunity cells serve as a bridge to adaptive immunity cells including T helper 1 cells, cytotoxic T cells and resident memory T cells. IFN-γ is the primary cytokine mediator that activates the JAK/STAT pathway, causing keratinocytes to produce the key chemokines CXCL9 and CXCL10. Complex interactions between immune and non-immune cells finally result in apoptosis of melanocytes. This paper summarizes current knowledge on the etiological and genetic factors that contribute to vitiligo, with a focus on immunopathogenesis and the key cellular and cytokine players in the disease's inflammatory pathways.
Indexed as
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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.