Clinical Features, Immunopathogenesis, and Therapeutic Strategies in Vitiligo

Abstract

Vitiligo is an autoimmune disease of the skin characterized by epidermal melanocyte loss resulting in white patches, with an approximate prevalence of 0.5-2% worldwide. Several precipitating factors by chemical exposure and skin injury present commonly in patients with vitiligo. Although the diagnosis appears to be straightforward for the distinct clinical phenotype and specific histological features, vitiligo provides many challenges including chronicity, treatment resistance, frequent relapse, associated profound psychosocial effect, and negative impact on quality of life. Multiple mechanisms are involved in melanocyte disappearance, including genetics, environmental factors, and immune-mediated inflammation. Compelling evidence supports the melanocyte intrinsic abnormalities with poor adaptation to stressors leading to instability and release of danger signals, which will activate dendritic cells, natural killer cells, and innate lymphoid cells to initiate innate immunity, ultimately resulting in T-cell mediated adaptive immune response and melanocyte destruction. Importantly, the cross-talk between keratinocytes, melanocytes, and immune cells, such as interferon (IFN)-γ signaling pathway, builds inflammatory loops that give rise to the disease deterioration. Improved understanding of the immune pathogenesis of vitiligo has led to the development of new therapeutic options including Janus kinase (JAK) inhibitors targeting IFN-γ signaling pathways, which can effectively reverse depigmentation. Furthermore, definition of treatment goals and integration of comorbid diseases into vitiligo management have revolutionized the way vitiligo is treated. In this review, we highlight recent developments in vitiligo clinical aspects and immune pathogenesis. Our key objective is to raise awareness of the complexity of this disease, the potential of prospective therapy strategies, and the need for early and comprehensive management.

Expression Profile and Bioinformatics Analysis of Circular RNAs in Patients with Vitiligo

“…The patients involved in this study were consistent with the diagnostic criteria of vitiligo. 2 Systemic therapy (glucocorticoids, immunosuppressive agents, and biological agents), phototherapy, or topical therapy (corticosteroid agents, vitamin D analogs, and tacrolimus) were not used within 3 months before the collection of specimens. No congenital diseases, acquired autoimmune diseases, other immune-related diseases, coagulation disorder, or other inappropriate surgical diseases were reported.…”

“… 1 The estimated global prevalence of vitiligo varies from 0.5% to 2%. 2 The clinical classification of vitiligo is generally divided into non-segmental, segmental, mixed and undetermined types. The former includes generalized, universal, acrofacial and mucosal types.…”

Vitiligo: Pathogenesis, Clinical Features, and Treatment

“…Vitiligo is classified as an autoimmune disease having a genetic basis and an association with environmental factors, including chemical triggers, skin injury, sunburn, and virus infection. Vitiligo is considered to develop as a result of metabolic, oxidative stress, and cell detachment abnormalities [7,8].…”

Sesquiterpenoids from Seriphidium transiliense and Their Melanogenic Activity

“…10−12 However, an adaptive immune response inducing melanocyte destruction mediated by IFN-γ-JAK/STAT-chemokine signaling is being recognized increasingly as a main reason for vitiligo. 13,14 The IFN-γchemokine signaling axis is responsible for recruiting autoimmune cells to kill melanocytes, which involves Janus kinase (JAK) 1 and 2, chemokine (C-X-C motif) ligand (CXCL) 9 and 10, and phospho-signal transducers and activators of transcription (p-STAT). It is reported that the biomarker for the progression of vitiligo is chemokine CXCL10, which is identified as playing a critical role in both the progression and maintenance of vitiligo.…”

“…Therefore, the absolute configuration of 2 (seritranin B) was determined as 7Z,10S. Quantum chemical calculations showed (7Z,10S)-2 exhibited an excellent linear correlation between the experimental and calculated 13 C and 1 H NMR chemical shifts (R 2 : C 0.99868; 1 H 0.99580) (Figure S2C and D, Supporting Information). In addition, the CMAE and MD of 13 C for (7Z,10S)-2 were 1.78 and 4.90 (Table S5, Supporting Information), which conformed to the standard MAE < 2.2 and MD < 5.…”