Taken together, our results demonstrate that oxidative stress-induced IL-15 trans-presentation in keratinocytes contributes to the activation of CD8<sup>+</sup> T<sub>EMs</sub>, providing a novel mechanism by which oxidative stress initiates autoimmunity in vitiligo.
Given the prominent role of nicotinamide adenine dinucleotide (NAD<sup>+</sup>)-dependent deacetylase Sirtuin3 (SIRT3) in sustaining mitochondrial dynamics and homeostasis and that SIRT3 expression and activity can be influenced by oxidative stress-related signaling, we wondered whether SIRT3 could play an important role in vitiligo melanocyte degeneration by regulating mitochondrial dynamics.
MicroRNA‑155 (miR‑155) is known to contribute to the pathogenesis of vitiligo; however, the mechanism by which miR‑155 regulates the development of vitiligo remains unclear.
The aim of this study is to investigate keratinocytes' role in vitiligo pathogenesis through immunohistochemical expression of LXR-α in lesional, perilesional, and distant nonlesional vitiligo skin.
Expression of NRG1 was significantly less in lesional dermis of vitiligo patients as compared to nonlesional and healthy control dermis both at mRNA as well as protein level.
Focusing on this interplay, we have reviewed existing literature supporting evidence on cellular and functional alterations of surrounding epidermal keratinocytes, extracellular matrix (ECM) proteins and fibroblasts in the underlying dermal compartment that may contribute to melanocyte disappearance in vitiligo.
The aim of this study was to explore the mechanism underlying CO2 fractional laser treatment of vitiligo by detecting the levels of Th1 cytokines (IL-2 and IFN-γ), Th2 cytokines (IL-4 and IL-10), and Th17 cytokines (IL-17 and IL-23) in peripheral blood.
The aim of this study was to evaluate the possible associations between the +405 G/C single nucleotide polymorphisms (SNP) of the VEGF gene (rs2010963) and vitiligo.
Additionally, enrichment analysis suggested that targets of KBL on vitiligo were mainly clustered into multiple biological processes (associated with DNA translation, lymphocyte differentiation and activation, steroid biosynthesis, autoimmune and systemic inflammatory reaction, neuron apoptosis, and vitamin deficiency) and related pathways (TNF, JAK-STAT, ILs, TLRs, prolactin, and NF-<i>κ</i>B), indicating the underlying mechanisms of KBL on vitiligo.
Panniculitis and vitiligo occurring during BRAF and MEK inhibitors combination in advanced melanoma patients: Potential predictive role of treatment efficacy.
A similar experiment was performed using further homeopathic preparations sourced from kojic acid (KA), hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>; HP), 6-biopterin (BP), and [Nle<sup>4</sup>, D-Phe<sup>7</sup>]-α-melanocyte-stimulating hormone (NLE), some of which are known to induce vitiligo or melano-destruction at physiological dose.
Among these metabolites and proteins, lysophosphatidylcholine, platelet-activating factor, sn-glycerol-3-phosphocholine, succinic acid, CXCL4 and CXCL7 were significantly elevated in the plasma of patients with vitiligo, while aspartate was downregulated.
Results: Baseline LGI3 immunohistochemical studied parameters (expression, intensity, percentage and H score) were significantly lower in vitiligo cases than controls (p=0.003, 0.013, 0.001 and 0.001 respectively).
HSP70i is secreted by stressed melanocytes, is associated with human vitiligo lesions, and functionally contributes to a mouse model of vitiligo.Henning et al. report that treatment with a modified version of the protein reversed depigmentation in Sinclair swine, a useful animal model of vitiligo.
The western blotting results showed that Peroxiredoxin‑6, apolipoprotein L1, apolipoprotein E and mannose‑binding protein were differentially expressed in patients with different stages of vitiligo.