The Immunogenetics of Vitiligo: An Approach Toward Revealing the Secret of Depigmentation

Dwivedi, Mitesh; Laddha, Naresh C.; Begum, Rasheedunnisa

doi:10.1007/978-3-030-92616-8_3

Cited by 3 publications

(2 citation statements)

References 254 publications

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“…Of note, cumulative evidence from vitiligo mouse models [53,54] and human vitiligo skin biopsies [55,56] shows that key players in vitiligo pathogenesis include hyperactive IFN-γ signaling pathways and activated pathways involving cytotoxic CD8+ T lymphocytes [57][58][59][60] (Figure 2). GWAS from vitiligo patients (mainly from a European-derived white population and Han Chinese population) identified 50 confirmed loci that included CTLA4, interferon regulatory factor 4 (IRF4), MHC class 1 (HLA-A, HLA-B, and HLA-C), MHC class 2 (HLA-DRB1, HLA-DQA1, HLA-DQB1, and HLA-DRA), zinc finger protein Eos (IKZF4; transcription factor expressed in regulatory T lymphocytes), and GZMB [2,61]. These genes associated with immune modulations may serve as susceptibility/risk biomarkers for vitiligo.…”

Section: Pathogenesis Of Vitiligomentioning

confidence: 99%

“…Autophagy is activated in melanocytes and fibroblasts that reside in adjacent vitiligo non-lesions to antagonize degenerative stress, indicating the premature senescent status of these cells [68]. Additionally, impaired autophagy increases CXCL16 secretion GWAS from vitiligo patients (mainly from a European-derived white population and Han Chinese population) identified 50 confirmed loci that included CTLA4, interferon regulatory factor 4 (IRF4), MHC class 1 (HLA-A, HLA-B, and HLA-C), MHC class 2 (HLA-DRB1, HLA-DQA1, HLA-DQB1, and HLA-DRA), zinc finger protein Eos (IKZF4; transcription factor expressed in regulatory T lymphocytes), and GZMB [2,61]. These genes associated with immune modulations may serve as susceptibility/risk biomarkers for vitiligo.…”

Section: Pathogenesis Of Vitiligomentioning

confidence: 99%

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Pathogenesis of Alopecia Areata and Vitiligo: Commonalities and Differences

Yamaguchi,

Peeva

2024

IJMS

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Both alopecia areata (AA) and vitiligo are distinct, heterogenous, and complex disease entities, characterized by nonscarring scalp terminal hair loss and skin pigment loss, respectively. In AA, inflammatory cell infiltrates are in the deep reticular dermis close to the hair bulb (swarm of bees), whereas in vitiligo the inflammatory infiltrates are in the epidermis and papillary dermis. Immune privilege collapse has been extensively investigated in AA pathogenesis, including the suppression of immunomodulatory factors (e.g., transforming growth factor-β (TGF-β), programmed death-ligand 1 (PDL1), interleukin-10 (IL-10), α-melanocyte-stimulating hormone (α-MSH), and macrophage migration inhibitory factor (MIF)) and enhanced expression of the major histocompatibility complex (MHC) throughout hair follicles. However, immune privilege collapse in vitiligo remains less explored. Both AA and vitiligo are autoimmune diseases that share commonalities in pathogenesis, including the involvement of plasmacytoid dendritic cells (and interferon-α (IFN- α) signaling pathways) and cytotoxic CD8+ T lymphocytes (and activated IFN-γ signaling pathways). Blood chemokine C-X-C motif ligand 9 (CXCL9) and CXCL10 are elevated in both diseases. Common factors that contribute to AA and vitiligo include oxidative stress, autophagy, type 2 cytokines, and the Wnt/β-catenin pathway (e.g., dickkopf 1 (DKK1)). Here, we summarize the commonalities and differences between AA and vitiligo, focusing on their pathogenesis.

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Section: Pathogenesis Of Vitiligomentioning

confidence: 99%

Section: Pathogenesis Of Vitiligomentioning

confidence: 99%

Pathogenesis of Alopecia Areata and Vitiligo: Commonalities and Differences

Yamaguchi,

Peeva

2024

IJMS

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Identification of Coding Variants in 10q22.1 Associated with Vitiligo in the Chinese Han Population

Tang,

Cheng,

Cheng

et al. 2024

Genetic Testing and Molecular Biomarkers

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An Overview of the Biological Complexity of Vitiligo

Matarrese,

Puglisi,

Mattia

et al. 2024

Oxidative Medicine and Cellular Longevity

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Vitiligo is a skin disease that affects all ethnicities and genders and is characterized by the loss of pigment essentially due to the selective loss of melanocytes. Although it is generally considered a systemic disease associated with polymorphisms in genes involved in the immune response, vitiligo is also considered an oxidative imbalance‐associated disease. It represents a multifactorial pathology in which some genetic predisposition and epigenetic factors coupled with some critical biochemical and molecular pathways could play a pivotal role. The aim of this work was thus to review some of the fine cellular mechanisms involved in the etiopathogenesis of vitiligo, mainly focusing on the nonimmunological ones, extensively highlighted elsewhere. We took into consideration, in addition to oxidative stress, both the cause and the hallmark of the pathology, some less investigated aspects such as the role of epigenetic factors, e.g., microRNAs, of receptors of catecholamines, and the more recently recognized role of the mitochondria. Sex differences associated with vitiligo have also been investigated starting from sex hormones and the receptors through which they exert their influence. From literature analysis, a picture seems to emerge in which vitiligo can be considered not just a melanocyte‐affecting disease but a systemic pathology that compromises the homeostasis of a complex tissue such as the skin, in which different cell types reside playing multifaceted physiological roles for the entire organism. The exact sequence of cellular and subcellular events associated with vitiligo is still a matter of debate. However, the knowledge of the individual biological factors implicated in vitiligo could help physicians to highlight useful innovative markers of progression and provide, in the long run, new targets for more tailored treatments based on individual manifestations of the disease.

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The Immunogenetics of Vitiligo: An Approach Toward Revealing the Secret of Depigmentation

Cited by 3 publications

References 254 publications

Pathogenesis of Alopecia Areata and Vitiligo: Commonalities and Differences

Pathogenesis of Alopecia Areata and Vitiligo: Commonalities and Differences

Identification of Coding Variants in 10q22.1 Associated with Vitiligo in the Chinese Han Population

An Overview of the Biological Complexity of Vitiligo

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