The Role of CXCL10 and IL-18 as Markers of Repigmentation Response in Nonsegmental Vitiligo Treated with Narrowband UVB Phototherapy: A Prospective Cohort Study

Hojman, Lía; Cabrera, Raúl; Karsulovic, Claudio; Tempio, Fabián; Pérez, Claudio; López, Mercedes

doi:10.1016/j.jid.2020.12.021

Cited by 6 publications

(5 citation statements)

References 12 publications

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“… 25 , 26 CXCL10 is dominant over CXCL9 in vitiligo and HT. 27 , 28 CXCL9 recruits the immune cells while CXCL10 mediates the migration and localization of melanocyte-specific CD8 + T cells to the epidermis. 20 CXCL10 is correlated with disease severity, activity, treatment response, and outcome in vitiligo.…”

Section: Discussionmentioning

confidence: 99%

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Identification of Shared Biomarkers and Immune Infiltration Signatures between Vitiligo and Hashimoto’s Thyroiditis

Lu,

Song,

Luan

et al. 2024

CCID

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Background Vitiligo and Hashimoto’s thyroiditis (HT) are concomitant autoimmune diseases characterized by the destruction of melanocytes or thyrocytes. We aimed to explore the immunological mechanism of this comorbidity and screen their potential biomarkers. Methods We downloaded the microarray datasets from the GEO database. Differentially expressed genes (DEGs) and immune-related genes (IRGs) were selected. The immune-related differentially expressed genes (IRDEGs) were obtained by taking the intersection. Candidate biomarkers were elected by Cytoscape software. CIBERSORT was used to depict immune cell infiltration prospects. Correlation analysis was conducted between infiltrating cells and several indicators. The results were validated by real-time quantitative PCR (RT-qPCR). Results Three datasets and 60 IRDEGs were obtained in total. Pathway enrichment analysis showed that the T cell receptor signaling pathway, IL-17 signaling pathway, receptor-ligand activity, and signaling receptor activator activity were significantly enriched. We screened out four hub genes, including IFNG , STAT1 , IL1B , and CXCL10 . The ROC curve indicated the highest diagnostic value of CXCL10 in both vitiligo and HT. Immuno-infiltration analysis revealed significant changes in T cell subsets and macrophage subtypes, which were correlated with four hub genes, melanocyte markers, and thyroid-specific antigens. qPCR validated the hub genes in peripheral blood mononuclear cells from patients with comorbidity. Conclusion IFNG , STAT1 , IL1B , and CXCL10 , were the key IRDEGs to vitiligo and HT. These genes may participate in the comorbidity by remodeling the immune cell infiltration pattern, and cross-expressed antigens may mediate the common damage of melanocytes and thyroid tissues.

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Section: Discussionmentioning

confidence: 99%

“…25,26 CXCL10 is dominant over CXCL9 in vitiligo and HT. 27,28 CXCL9 recruits the immune cells while CXCL10 mediates the migration…”

Section: Discussionmentioning

confidence: 99%

Identification of Shared Biomarkers and Immune Infiltration Signatures between Vitiligo and Hashimoto’s Thyroiditis

Lu,

Song,

Luan

et al. 2024

CCID

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“…This is consistent with another study reporting decreased CXCL10 amounts by averagely 42% following NB‐UVB therapy for 24 sessions. 16 CXCL10 is one of the most reliable serum biomarkers of vitiligo activity. 17 IFN‐g is critical for CXCL10 secretion and contributes to CD8 + T‐cell recruitment to injured skin via CXCR3.…”

Section: Discussionmentioning

confidence: 99%

Altered circulating memory T cells in vitiligo cases followed NB‐UVB therapy

Lin

Sun

Lei

et al. 2021

Photoderm Photoimm Photomed

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Vitiligo represents a chronic skin depigmenting pathology featuring melanocyte depletion in the epidermis, affecting 0.5% to 2% of the general population. Vitiligo involves polymorphisms in genes responsible for immune responses and melanogenesis. Altered inflammatory and immune responses are considered the essential mechanisms inducing the dysfunction and death of melanocytes. 1 Direct injury of melanocytes is mostly induced by CD8+ T cells. 2 Other subsets of T cells, especially memory T cells, are also involved in the development, maintenance, and flares of vitiligo.Vitiligo is currently considered a memory skin disease. 3 Following

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“…UVB decreased migration of Langerhans cells, decreased the expression of stimulatory signals in dendritic cells, and restored regulatory T cells [13]. Moreover, UVB-irradiated T cells progressed to apoptosis in 20 h in an in vitro study [23], and the level of C-X-C motif chemokine ligand (CXCL10) and circulating interferon (IFN)-γ+ CD8+ T cells were significantly decreased after 24 sessions of NBUVB in patients with vitiligo [24]. UV-induced apoptosis of CD4+ and CD8+ T cells may lead to the elimination of cytotoxic T cells and resident memory T cells allowing melanocytes to repopulate (shown in Fig.…”

Section: Phototherapymentioning

confidence: 99%

Bridging Molecular Mechanism and Clinical Practice in Vitiligo Treatment: An Updated Review

Ju,

Bae

2024

Dermatology

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Background: In recent years, a great advance has been made in the area of pathogenesis of vitiligo and the understanding of vitiligo treatment is also expanding. Summary: Treatment of vitiligo seeks to achieve three goals: cessation of disease progression, regeneration of pigmentation, and prevention of recurrence. To achieve these goals, a number of non-surgical interventions are available that suppress the autoimmune response and regenerate the remaining melanocytes from the reservoir, and optimal treatment outcome can be achieved when each modality is used properly. Key Messages: Our review describes various treatment modalities for vitiligo based on their molecular mechanism of action. Bridging the gap between molecular mechanisms and therapeutic options would be a valuable reference for physicians in clinical practice.

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The Role of CXCL10 and IL-18 as Markers of Repigmentation Response in Nonsegmental Vitiligo Treated with Narrowband UVB Phototherapy: A Prospective Cohort Study

Cited by 6 publications

References 12 publications

Identification of Shared Biomarkers and Immune Infiltration Signatures between Vitiligo and Hashimoto’s Thyroiditis

Identification of Shared Biomarkers and Immune Infiltration Signatures between Vitiligo and Hashimoto’s Thyroiditis

Altered circulating memory T cells in vitiligo cases followed NB‐UVB therapy

Bridging Molecular Mechanism and Clinical Practice in Vitiligo Treatment: An Updated Review

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