ArticleCells2023
Pathogenic Th2 Cytokine Profile Skewing by IFN-γ-Responding Vitiligo Fibroblasts via CCL2/CCL8.
Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Evaluation ofMedicina (Kaunas, Lithuania) · 2023Pooled it
- Combination of Baricitinib and Phototherapy in Adults With Active Vitiligo: A Randomized Clinical Trial.JAMA dermatology · 2025Trial
- CD11c+ CD8 T cells cause IFN-γ-dependent autoimmune neuroinflammation that is restrained by PD-1 signaling.JCI insight · 2026Article
- Vitiligo as a Failure of Immune Resolution and Tissue Regeneration: From Stress Signals to Targeted Immune Modulation.Clinical reviews in allergy & immunology · 2026Review
- Histone demethylase JMJD1A protects mice from enteric bacterial infection by upregulating CCL8 expression to recruit macrophages and CD4+ T cells.PLoS pathogens · 2026Article
- Immune control of functional memory CD8 T cells in normal-appearing vitiligo skin.Science advances · 2025Article
- Characterization of Ets-1 deficiency-induced depigmentation in a mouse model: insights into vitiligo pathogenesis.Laboratory animal research · 2025Article
- A Scoping Review of Pathogenesis, Current Treatments, and Novel Approaches for Vitiligo.Journal of cosmetic dermatology · 2025Article
- Deciphering Depigmentation: Mouse Models for Vitiligo Research.The Journal of investigative dermatology · 2025Review
- Exosomal miR-493-3p Promote the Secretion of CXCL10 by Suppressing Keratinocyte Autophagy in Vitiligo.Clinical, cosmetic and investigational dermatology · 2025Article
- Role of fibroblasts in nonfibrotic autoimmune skin diseases.Molecular medicine (Cambridge, Mass.) · 2024Review
- Fibroblast: A Novel Target for Autoimmune and Inflammatory Skin Diseases Therapeutics.Clinical reviews in allergy & immunology · 2024Review
- Biologic drugs induced vitiligo: case reports and review of literature.Frontiers in immunology · 2024Review
- The role of dermal fibroblasts in autoimmune skin diseases.Frontiers in immunology · 2024Review
- Exploring mechanisms of skin aging: insights for clinical treatment.Frontiers in immunology · 2024Review
- A Mendelian randomization study on the causal effects of circulating cytokines on the risk of vitiligo.Frontiers in medicine · 2024Article
- Early short-term hypoxia promotes epidermal cell migration by activating the CCL2-ERK1/2 pathway and epithelial-mesenchymal transition during wound healing.Burns & trauma · 2024Article
- Type-2 immunity associated with type-1 related skin inflammatory diseases: friend or foe?Frontiers in immunology · 2024Review
- Aetiopathogenesis of Vitiligo.Dermatology practical & conceptual · 2023Review
- 1,25-Dihydroxyvitamin DNutrients · 2023Article
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
No grant is acknowledged in the PubMed record.
Abstract
purposeVitiligo is a T cell-mediated skin depigmentation disease. Though treatments arresting disease progression and inducing repigmentation are available, the efficacy of these options is often limited and poorly sustained. How stromal signals contribute to the interferon-γ-dominant skin niches is unclear. This study aims to determine how fibroblasts participate in the IFN-γ-dominant vitiligo niche. PATIENTS AND
methodsMouse vitiligo models were established. Fibroblasts from control and vitiligo mice were extracted for RNA sequencing. In vitro IFN-γ stimulation was performed to verify the JAK-STAT pathway by qPCR and Western blot. T cell polarization with chemokines was measured by flow cytometry. Protein levels in tissues were also examined by IHC.
resultsThe vitiligo mouse model recapitulates the human CD8-IFN-γ pathway. RNA sequencing revealed elevated chemokine CCL2 and CCL8 in vitiligo fibroblast, which may be regulated by the JAK-STAT signaling. Such phenomenon is verified by JAK inhibitor peficitinib in vitro. Moreover, CCL2 addition into the naïve T polarization system promoted type 2 cytokines secretion, which represents a hallmark of vitiligo lesions.
conclusionDermal fibroblasts, a principal constituent of skin structure, respond to IFN-γ by skewing T cells towards a type 2 cytokine profile via CCL2 and CCL8, which can be abrogated by JAK inhibitor peficitinib.
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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.