Levels of TNF-α, IL-6, IL-17, IL-37 cytokines in patients with active vitiligo

Karagün, Ebru; Baysak, Sevim

doi:10.1080/13685538.2020.1806814

Cited by 19 publications

(13 citation statements)

References 35 publications

(41 reference statements)

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“…Autophagic cell death rather than cell death with autophagy is another condition. Many studies have shown that the IL-17 level is higher in the serum and lesions of vitiligo patients compared to healthy individuals, suggesting its possible role in the pathogenesis of vitiligo [ 70 ]. The elevated IL-17 in lesions might contribute to the more autophagic vacuoles in melanocytes, and the autophagic process might be involved in the death of melanocytes in vitiligo by the IL-17 mediated ROS autophagy-associated cell apoptosis.…”

Section: Forms Of Melanocyte Death Induced By Oxidative Stress In Vitiligomentioning

confidence: 99%

The Role of Oxidative Stress in the Pathogenesis of Vitiligo: A Culprit for Melanocyte Death

Xuan

Yang

Xiang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Vitiligo is a common chronic acquired pigmentation disorder characterized by loss of pigmentation. Among various hypotheses proposed for the pathogenesis of vitiligo, oxidative stress-induced immune response that ultimately leads to melanocyte death remains most widely accepted. Oxidative stress which causes elevated levels of reactive oxygen species (ROS) can lead to dysfunction of molecules and organelles, triggering further immune response, and ultimately melanocyte death. In recent years, a variety of cell death modes have been studied, including apoptosis, autophagy and autophagic cell death, ferroptosis, and other novel modes of death, which will be discussed in this review in detail. Oxidative stress is also strongly linked to these modes of death. Under oxidative stress, ROS could induce autophagy by activating the Nrf2 antioxidant pathway of melanocytes. However, persistent stimulation of ROS might eventually lead to excessive activation of Nrf2 antioxidant pathway, which in turn will inactivate autophagy. Moreover, ferroptosis may be triggered by oxidative-related transcriptional production, including ARE, the positive feedback loop related to p62, and the reduced activity and expression of GPX4. Therefore, it is reasonable to infer that these modes of death are involved in the oxidative stress response, and that oxidative stress also acts as an initiator for various modes of death through some complex mechanisms. In this study, we aim to summarize the role of oxidative stress in vitiligo and discuss the corresponding mechanisms of interaction between various modes of cell death and oxidative stress. These findings may provide new ideas for exploring the pathogenesis and potential therapeutic targets of vitiligo.

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Section: Forms Of Melanocyte Death Induced By Oxidative Stress In Vitiligomentioning

confidence: 99%

The Role of Oxidative Stress in the Pathogenesis of Vitiligo: A Culprit for Melanocyte Death

Xuan

Yang

Xiang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…IL-6 is secreted by T lymphocytes and macrophages. Increased serum levels of IL-6 are reported in patients with vitiligo [ 52 ], in particular in those with new lesions [ 53 ]. Oxidative stress may influence IL-6 expression.…”

Section: Vitiligo Pathogenesis: Ab Origine Development From Gene To Cellular Dynamicsmentioning

confidence: 99%

“…IL-17 is a pro-inflammatory cytokine with a clear connection to numerous inflammatory diseases, such as psoriasis. Serum and tissue levels of IL-17 are higher in vitiligo patients than in controls [ 49 , 53 , 57 ] and a positive correlation was observed between IL-17 levels and the duration and body surface area (BSA) of the disease [ 52 , 57 ]. IL-17 cytokines are produced mainly by T helper 17 (Th17) cells, which are increased in the serum of patients with active vitiligo [ 58 ] and a positive correlation was also found between circulating Th17 cells and BSA, suggesting a role in progressive disease [ 59 ].…”

Section: Vitiligo Pathogenesis: Ab Origine Development From Gene To Cellular Dynamicsmentioning

confidence: 99%

“…Although JAK1/2 inhibition seems to be a better treatment option compared to JAK1/3 inhibition by tofacitinib, the results obtained from a randomized trial [ 105 ] showed comparable effects, whereas other case reports [ 106 , 107 ] have confirmed a lack of significant improvement. As mentioned, IL-6 is implicated in the immunopathogenesis of vitiligo, in particular in active disease [ 53 ]. Tocilizumab is an anti -interleukin -6 (IL -6) receptor humanized monoclonal antibody, approved for the treatment of rheumatoid arthritis and juvenile idiopathic arthritis (JIA).…”

Section: Vitiligo Treatment Options: Past Present and Future Therapiesmentioning

confidence: 99%

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Role of Cytokines in Vitiligo: Pathogenesis and Possible Targets for Old and New Treatments

Custurone

Bartolomeo

Irrera

et al. 2021

IJMS

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Vitiligo is a chronic autoimmune dermatosis of which the pathogenesis remains scarcely known. A wide variety of clinical studies have been proposed to investigate the immune mediators which have shown the most recurrency. However, such trials have produced controversial results. The aim of this review is to summarize the main factors involved in the pathogenesis of vitiligo, the latest findings regarding the cytokines involved and to evaluate the treatments based on the use of biological drugs in order to stop disease progression and achieve repigmentation. According to the results, the most recurrent studies dealt with inhibitors of IFN-gamma and TNF-alpha. It is possible that, given the great deal of cytokines involved in the lesion formation process of vitiligo, other biologics could be developed in the future to be used as adjuvants and/or to entirely replace the treatments that have proven to be unsatisfactory so far.

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“…Higher levels of IL-17A level in skin and serum of patients with vitiligo have also been found [5,18,19]. On the other hand, IL-17 + cells were detected in lesional and perilesional skin [14,20,21] in addition to in ltration of these cells into the upper dermis in patients with vitiligo [14,20].Positive correlations between vitiligo and early age of onset, disease duration, affected body surface area [14,22,23], and disease progression have been found [5,14,16,24,25].…”

Section: Introductionmentioning

confidence: 99%

Association of rs4711998 of IL-17A, rs2275913 of IL-17A and rs763780 IL-17F gene polymorphisms with vitiligo in a Mexican population

Ocampo‐Candiani

Salazar

Kubelis‐López

et al. 2022

Preprint

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Vitiligo is the most common depigmenting disease characterized by achromic macules due to selective loss of melanocytes. The pathogenesis remains poorly elucidated, and multiple hypotheses exists regarding its pathogenesis. Evidence suggests that stress on melanocytes can result in activation of the immune system, and involvement of both activated cluster of differentiation (CD8+) cytotoxic and CD4 + T-cells in the dysfunction, depigmentation, and apoptosis of melanocytes. Recent studies show that the interleukin 17 (IL-17) axis plays a central role in the pathogenesis of the disease. IL-17 is an important regulatory effector cytokine in this pathway. The aim of this study was to evaluate the association of IL-17A rs4711998 (-832A/G), IL-17A rs2275913 (-197G/A), and IL-17F rs763780 (7488A/G) with vitiligo in a Northeastern Mexican population. This study was a case-control study and included 116 patients with vitiligo and 116 control subjects. Genotype characterization of IL-17A rs4711998 (-832A/G), IL-17A rs2275913 (-197G/A), and IL-17F rs763780 (7488A/G) was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. A P ≤ 0.05 was considered significant. It was observed that the combination of the genotypes GG/GA for IL-17F rs763780 (7488A/G) were associated with an increased risk for the development of vitiligo (OR = 2.0943, 95% Cl 1.2375–3.5445, P = 0.0056). Regarding IL-17A genotyping rs4711998 (-832A/G) and IL-17A rs2275913 (-197G/A), no association with vitiligo development was found. In conclusion, the SNP rs763780 in the IL-17F gene appears to be a risk factor for vitiligo development in this Mexican population.

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Levels of TNF-α, IL-6, IL-17, IL-37 cytokines in patients with active vitiligo

Cited by 19 publications

References 35 publications

The Role of Oxidative Stress in the Pathogenesis of Vitiligo: A Culprit for Melanocyte Death

The Role of Oxidative Stress in the Pathogenesis of Vitiligo: A Culprit for Melanocyte Death

Role of Cytokines in Vitiligo: Pathogenesis and Possible Targets for Old and New Treatments

Association of rs4711998 of IL-17A, rs2275913 of IL-17A and rs763780 IL-17F gene polymorphisms with vitiligo in a Mexican population

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