Oxidized tyrosinase: A possible antigenic stimulus for non-segmental vitiligo autoantibodies

Al‐Shobaili, Hani A.; Rasheed, Zafar

doi:10.1016/j.jdermsci.2015.06.009

Cited by 26 publications

(20 citation statements)

References 56 publications

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“…Severe changes in tyrosinase conformation and function were observed with ROS effect. IgG‐type autoantibodies obtained from patients with vitiligo bound more strongly to oxidised tyrosinase compared with healthy volunteers 46 . In addition, there was a significant association between IgG antibody levels and disease severity.…”

Section: Discussionmentioning

confidence: 87%

“…Reactive oxygen species (ROS) may also play a role in vitiligo pathogenesis by stimulating change in melanocytic antigens and new antigen formation. Al‐Shobaili et al investigated ROS‐induced modified‐ tyrosinase (oxidised tyrosinase, ROR‐tyrosinase) as a possible antigenic stimulator in non‐segmental vitiligo 46 . The binding properties of antibodies to oxidised tyrosinase were evaluated comparatively in patients with vitiligo with different disease duration and severity and in healthy controls.…”

Section: Discussionmentioning

confidence: 99%

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The relationship between non‐segmental Vitiligo, HLA genotype and oxidative stress

2021

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Background Vitiligo is an autoimmune disease characterised by acquired loss of melanocytes. Although the pathogenesis of vitiligo remains unknown, oxidative stress and autoimmune dysregulations are considered to play a role. Objective The aim of this study was to evaluate the HLA profile and total antioxidant capacity (TAC) and their relationship to clinical characteristic of vitiligo patients. Methods Ninety‐one vitiligo patients and 100 healthy controls were included in the study. We analysed HLA allele frequencies using sequence‐specific oligonucleotide Prob (SSOP) method. Serum total antioxidant capacity (TAC) levels were measured and compared between vitiligo patients and controls. Results HLA‐A*02 allele frequency was increased (OR = 1.6, CI = 1.12‐2.24, P = .009), HLA‐A*11 (OR = 0.46, CI = 0.32‐0.91, P = .019) and HLA‐DRB1*01 (OR = 0.39, CI = 0.16‐0.92, P = .029) frequencies were decreased in vitiligo patients. HLA‐A*02 allele especially increased the risk of late onset (Vitiligo onset >30 years of age) vitiligo (OR:3.67, 95% CI: 1.63‐8.26, P = .002). Serum TAC levels were similar between vitiligo patients and healthy controls but TAC levels were significantly lower in patients who did not have an HLA‐DRB1*01 allele (1.52 vs 1.61, P = .033). Conclusion Our study showed that HLA‐A*02 increases, HLA‐A*11 and HLA‐DRB1*01 decreases vitiligo susceptibility in Turkish patients as well as a possible relationship between HLA and TAC.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

The relationship between non‐segmental Vitiligo, HLA genotype and oxidative stress

2021

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“…Oxidative stress and autoimmunity with genetic susceptibility have been associated with the pathogenesis of AA and vitiligo [2,[18][19][20]. The correlation between those two pathways 2…”

Section: Discussionmentioning

confidence: 99%

Increased Serum Levels of IFN-γ, IL-1β, and IL-6 in Patients with Alopecia Areata and Nonsegmental Vitiligo

Tomaszewska

Kozłowska

Kaszuba

et al. 2020

Oxidative Medicine and Cellular Longevity

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Alopecia areata (AA) and vitiligo are both common skin diseases of autoimmune origin. Both alopecia areata and vitiligo have shown to be affected by oxidative stress. The present work is aimed at evaluating and comparing the serum proinflammatory cytokine levels in AA and nonsegmental vitiligo (NSV). A cross-sectional study was conducted of 33 patients with AA, 30 patients with NSV, and 30 healthy controls. Serum levels of interferon γ (IFN-γ), interleukin- (IL-) 1β, and IL-6 were determined quantitatively by ELISA method. Our analysis identified a signature of oxidative stress associated with AA and NSV, characterized by elevated levels of IFN-γ (AA: p=0.007283; NSV: p=0.038467), IL-1β (AA; NSV: p≤0.001), and IL-6 (AA; NSV: p≤0.001). IL-6 was also significantly increased in NSV patients in comparison with AA patients (p=0.004485). Our results supported the hypothesis that oxidative stress may play a significant role in promoting and amplifying the inflammatory process both in AA and vitiligo. The complex understanding of both disease etiopathogenesis involves interrelationships between oxidative stress and autoimmunity. The clinical study registration number is RNN/266/16/KE.

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“…From the inner stressor perspective, ROS can be attributed to a series of cellular metabolic processes which have an inherited incapacity to be resolved, such as melanogenesis, cellular proliferation/differentiation/apoptosis, and immune reactions [8]. Melanogenesis performed by melanocytes is an energy-consuming process, producing large quantities of pigment melanin [3], that can create a highly pro-oxidant environment in the epidermis [9,10].…”

Section: Sources Of Ros Overproduction In Vitiligomentioning

confidence: 99%

Perspectives of New Advances in the Pathogenesis of Vitiligo: From Oxidative Stress to Autoimmunity

2019

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Vitiligo is an autoimmune cutaneous disease in which melanocytes are destroyed by CD8 + T cells resulting in disfiguring white spots. From the very beginning of the disease, oxidative stress plays a significant role in promoting the onset of vitiligo, as noted by many studies. Multiple factors lead to the overproduction of reactive oxygen species (ROS), and collaboratively cause ROS accumulation in vulnerable melanocytes. However, ROS are responsible for melanocyte damage manifested by the level of molecules, organelles, and cells, and the generation of autoantigens, through different pathways related to the dysregulation of melanocytes. Recent studies have shown that presentation of autoantigens is mediated by innate immunity, which bridges the gap between oxidative stress and adaptive immunity. The recruitment of CD8 + T cells induced by cytokines and chemokines guarantees the final destruction of epidermal melanocytes. Moreover, emerging concerns regarding regulatory T cells and resident memory T cells help explain the reinstatement and relapse of vitiligo. Here, we provide new perspectives in the advances in understanding of this disease pathogenesis and we attempt to find more interrelationships between oxidative stress and autoimmunity.

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Oxidized tyrosinase: A possible antigenic stimulus for non-segmental vitiligo autoantibodies

Cited by 26 publications

References 56 publications

The relationship between non‐segmental Vitiligo, HLA genotype and oxidative stress

The relationship between non‐segmental Vitiligo, HLA genotype and oxidative stress

Increased Serum Levels of IFN-γ, IL-1β, and IL-6 in Patients with Alopecia Areata and Nonsegmental Vitiligo

Perspectives of New Advances in the Pathogenesis of Vitiligo: From Oxidative Stress to Autoimmunity

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