Translational Research in Vitiligo

Katz, Erica L.; Harris, John E.

doi:10.3389/fimmu.2021.624517

Cited by 38 publications

(45 citation statements)

References 193 publications

(260 reference statements)

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“…Vitiligo is an acquired, chronic skin pigmentary disorder, characterized by progressive loss of melanin and melanocytes in the epidermis [ 3 ]. The precise cause remains unknown, but an increasing number of observations highlight the important role of cellular immunity in the pathogenesis of this disease [ 5 , 30 ].…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it has been suggested that disruption of immune homeostasis is involved in vitiligo pathogenesis, although more studies are needed to test this hypothesis [ 5 ]. Clinically, doctors have noted that depigmented skin from patients with vitiligo does not develop contact dermatitis in response to sensitization with dinitrofluorobenzene (DNFB) [ 6 , 7 ], although pigmented skin from vitiligo patients responded normally.…”

Section: Introductionmentioning

confidence: 99%

“…Recently, it has been suggested that disruption of immune homeostasis is involved in vitiligo pathogenesis, although more studies are needed to test this hypothesis [5].…”

Section: Introductionmentioning

confidence: 99%

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Morphological Alterations and Increased S100B Expression in Epidermal Langerhans Cells Detected in Skin from Patients with Progressive Vitiligo

Yang

Teng

et al. 2021

Life

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The role of Langerhans cells (LCs) in vitiligo pathogenesis remains unclear, with published studies reporting contradictory results regarding the quantity of LCs and no data on the features of LCs in vitiligo. Here, we aimed to analyze the presence, density, and morphological features of LCs in the epidermis of patients with vitiligo. Skin biopsies were stained for LCs using anti-CD1a/anti-langerin antibodies and analyzed by immunocytochemistry with light and electron microscopy. Compared with healthy controls, we detected significantly increased numbers of epidermal LCs in lesional skin from vitiligo in the progressive state. These LCs exhibited striking morphological alterations, including an elevated number of dendrites, with increased length and more branches than dendrites from controls. Ultrastructure examination via immuno-electron microscopy revealed markedly reduced Birbeck granules (BGs) and shorter BG rods in LCs from progressive vitiligo, with higher expression of langerin. Additionally, expression of S100B, the activity biomarker of vitiligo, was increased in these LCs. This work provides new insight on the cellular composition of LCs in vitiliginous skin, revealing altered morphology and increased LC numbers, with elevated S100B expression. Our data suggest LCs might play a critical role in vitiligo pathogenesis and thus may represent a novel therapeutic target for this disease.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Morphological Alterations and Increased S100B Expression in Epidermal Langerhans Cells Detected in Skin from Patients with Progressive Vitiligo

Yang

Teng

et al. 2021

Life

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“…[7] A variety of hypotheses have been proposed to explain the pathophysiology of vitiligo. Innervation, microvascular anomalies, oxidative stressinduced melanocyte degeneration, problems in melanocyte adhesion, autoimmune, somatic mosaicism, and genetic factors are all included in these hypotheses [29][30][31][32][33][34][35][36]. The autoimmune hypothesis is presently the most commonly cited and researched among professionals.…”

Section: Pathophysiologymentioning

confidence: 99%

An Overview on the Epidemiology, Pathophysiology and Treatment of Vitiligo: A Review

Alenizi

Al-Ruwaili

Alanazi

et al. 2021

JPRI

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Vitiligo is one of the complex diseases that has existed during the entire history of humanity and so far we have not fully understood it, serval theories have been proposed most of them suggest strong linkage between deficiencies in certain genes and the disease, refereeing that the disease has strong genetic factor that plays a rule in triggering the disease, and the epidemiology studies confirms also that theory due to higher incidence in people who have siblings but this theory does not fully unlocks the full causes of the disease as it seems also to have strong environmental triggers. One of the biggest problem about the disease and the QoL is not the disease lifestyle itself but rather the social and psychological effects of the disease and the social acceptance impact, because it affects the appearance of its patients and thus affects their social acceptance leading to some serious psychological and depressive disorders, and that effects differs from society to another and by different categories, that’s why psychological follow up and treatment is critical part of the overall treatment. In this review, we overview recent updates in epidemiology, pathophysiology and treatment of vitiligo.

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“…Activated CD8 + T cells play a key role in the occurrence and progression of the disease [ 6 – 8 ]. Melanocyte-specific CD8 + T cells are recruited to the skin via chemokines, thereby releasing perforin, granzyme, and other cytotoxic substances that destroy the melanocytes [ 6 – 10 ]. However, the mechanism of CD8 + T cells to adhere to melanocytes is unknown.…”

Section: Introductionmentioning

confidence: 99%

Occludin Promotes Adhesion of CD8+ T Cells and Melanocytes in Vitiligo via the HIF-1α Signaling Pathway

Zou

Xiao

Deng

et al. 2022

Oxidative Medicine and Cellular Longevity

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Loss of melanocytes induced by activated CD8+ T cells is the pathological hallmark of vitiligo. Melanocyte-specific CD8+ T cells are recruited to the skin via chemokines, thereby releasing perforin, granzyme, and other cytotoxic substances that destroy the melanocytes. However, the mechanism of CD8+ T cells to adhere to melanocytes is unknown. Previous transcriptome sequencing results published by our group showed that the occluding (OCLN) gene was significantly upregulated in CD8+ T cells from skin lesions of vitiligo. Occludin is a crucial component of the tight junction between cells; in cells without tight junction, occludin mediates the adhesion of two cells in the form of a self-ligand. This study demonstrated that OCLN gene expression was elevated in the CD8+ T cells of vitiligo patients, and occludin mediates the adherence of CD8+ T cells to melanocytes. Besides, pathological changes in vitiligo skin lesions reveal that CD8+ T cells continuously persist in the skin lesions, which is related to the persistence of the disease. In this regard, we found that fibroblasts from vitiligo patients significantly express occludin, which may participate in the continuous retention of CD8+ T cells in the skin lesions. The pathogenesis of vitiligo is closely related to oxidative stress, and our data suggest that overexpression of hypoxia-inducible factor-1α (HIF-1α) increases the expression of occludin. Besides, ChIP-qPCR of CD8+ T cells revealed that HIF-1α directly binds to the OCLN promoter. Thus, occludin upregulation promotes the adhesion of CD8+ T cells and melanocytes via the HIF-1α signaling pathway. Our study results suggested a critical role for OCLN in the occurrence, progression, and maintenance of vitiligo. Therefore, inhibiting the expression of OCLN gene may be a potential targeted treatment strategy.

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Translational Research in Vitiligo

Cited by 38 publications

References 193 publications

Morphological Alterations and Increased S100B Expression in Epidermal Langerhans Cells Detected in Skin from Patients with Progressive Vitiligo

Morphological Alterations and Increased S100B Expression in Epidermal Langerhans Cells Detected in Skin from Patients with Progressive Vitiligo

An Overview on the Epidemiology, Pathophysiology and Treatment of Vitiligo: A Review

Occludin Promotes Adhesion of CD8+ T Cells and Melanocytes in Vitiligo via the HIF-1α Signaling Pathway

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