الفهرس 
Undetermined/unclassified vitiligoOnly 14 pages are availabe for public view
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Abstract
Vitiligo is a chronic idiopathic acquired disorder of pigmentation characterized by the development of white macules resulting from a loss of epidermal melanocytes (Boniface et al., 2018). The theories of the pathogenesis of vitiligo are focused on autoimmunity, mental stress, oxidative stress, metabolic toxins, and heredity (Jacquemin et al., 2019). Currently, the mechanisms thought to be involved in pigmentation loss in vitiligo include autoimmune dysfunction, neurotoxic factor destruction, and genetic factors (Kunchi et al., 2021).
An increasing number of studies suggest that the occurrence and progression of vitiligo are caused by multiple factors and are polygenic, and noncoding RNAs may play a vital role in an individual’s susceptibility to vitiligo (Mansuri et al., 2014).
Vitiligo affects approximately 1% of the population and can affect both adults and children, causing a diminished quality of life and marked psychological distress (Frisoli and Harris, 2017).
Long noncoding RNAs (lncRNAs) are defined as ncRNAs longer than 200 nucleotides without the capacity of coding proteins, located within the intergenic stretches or overlapping antisense transcripts of protein-coding genes (Wang et al., 2017). There is growing evidence that lncRNAs participate in various biological events, and many studies have suggested that dysregulation of lncRNAs is involved in the pathogenesis of autoimmune and inflammatory diseases (Lodde et al., 2020).
Nuclear enriched abundant transcript 1 (NEAT-1), a long noncoding RNA, is encoded on chromosome 11q13.1 and expresses constitutively and widely in many tissues and cell types (Sasaki et al., 2009). NEAT-1 may
participate in the immune dysregulation in Systemic Lupus Erythematosus (SLE) patients, by acting as a newly identified proinflammatory factor to facilitate the overproduction of cytokines and chemokines in a positive feedback manner (Zhang et al., 2016). A previous study researched the impact of NEAT-1 on Rheumatoid Arthritis (RA) and found that NEAT-1 expression in peripheral blood mononuclear cells of RA was increased obviously (Shui et al., 2019).
Interleukin 6 (IL-6) is an interleukin that acts as both a pro- inflammatory cytokine and an anti-inflammatory myokine. IL-6 stimulates the inflammatory and auto-immune processes in many diseases such as Multiple sclerosis (MS) and SLE (Tackey et al., 2014). IL-6 induces transcription of inflammatory genes and thus is implicated in a host of chronic disease conditions associated with inflammation and autoimmunity (Mihara et al., 2012).
IL-6 has a role in the transition from innate to acquired immunity. IL-6 can also create an immunological imbalance among Th17 and Treg cells bringing about an autoimmune pathology (Kimura and Kishimoto
2010). Elevated IL-6 expression is reported in the skin and serum of vitiligo patients (Farhan et al., 2014). Some studies point to the connection between the higher level of IL-6 in the tissue and/or serum and the presence of autoimmune disorders accompanying vitiligo (Alexandraki et al.,
2008).
Aim of work
Our study aimed to investigate the possible role of long non-coding RNA NEAT-1 and Interleukin-6 in the pathogenesis of vitiligo among a group of Egyptian patients