Increased Circulatory Interleukin-17A Levels in Patients with Progressive and Leukotrichial Vitiligo

Abstract

Background. Vitiligo is a chronic condition characterized by skin depigmentation. Although not life-threatening, it significantly impacts quality of life. The pathophysiology of vitiligo remains poorly understood, and treatment options are limited. Mounting evidence supports the importance of autoreactive T cells and, particularly interleukin-17A- (IL-17A-) secreting Th17 cells, in vitiligo. IL-17A targeting has been proven successful in various inflammatory dermatological conditions, including psoriasis and lupus erythematosus. Objective. We evaluated the relationship between serum levels of IL-17A and the clinicopathological characteristics of Vietnamese vitiligo patients. Methods. In this cross-sectional study, we analyzed data from 52 nonsegmental vitiligo patients and 50 age- and sex-matched healthy individuals. Serum levels of IL-17A were measured using an enzyme-linked immunosorbent assay. We evaluated the correlation between IL-17A levels and clinical characteristics including leukotrichia, disease duration, vitiligo activity, and body surface area involvement. Results. Patients with progressive vitiligo had significantly higher IL-17A levels than patients with stable vitiligo ( P = 0.014) or healthy individuals ( P = 0.002). In addition, serum IL-17A levels were higher in vitiligo patients with leukotrichia than in patients without it ( P = 0.04). Furthermore, serum IL-17A levels were negatively correlated with age (r = −0.39, P = 0.004) and age of onset (r = −0.33, P = 0.016) in vitiligo patients. Conclusions. Higher serum levels of IL-17A in patients with progressive vitiligo and leukotrichia suggest a potential role of IL-17A in melanocyte destruction in the epidermis and the follicular matrix.

Interleukin 38 serum level is increased in patients with vitiligo, correlated with disease severity, and associated with signs of disease activity

“…In this study, we also detected that serum level of IL‐38 was correlated negatively with the age of patients and the age of disease onset. Similarly, Le et al 17 demonstrated that serum IL‐17A level correlated negatively with the age of vitiligo patients and their age of disease onset. The authors assumed that the higher cytokine level in young patients might be caused by mental stress experienced by younger age groups, which plays a role in inducing vitiligo by exacerbating immunological dysregulation.…”

“…Furthermore, vitiligo activity was reported to be associated with overexpression of Th1 (TNF‐α and interferon‐γ 16 ) and Th17 cytokines (IL‐17A). 17 Taking together, the enhanced pro‐inflammatory cytokines in patients with signs of vitiligo activity might have further enhanced IL‐38 expression from monocytes and keratinocytes as an attempt to counteract the overexpression of these pro‐inflammatory cytokines. Indeed, signs of vitiligo activity have recently been recognized as crucial in clinical practice for initiating therapy to prevent disease progression 10…”

The role of cytokines and vitamin D in vitiligo pathogenesis

“…Th1 and Th17 cell activation pathway is one of the main autoimmune etiologies of vitiligo, 3 reinforced by reported raised or imbalanced level of IL‐17 in sera or skin biopsies of vitiligo patients, 4,38,44,47,61,62,75,87,93,94,102–105 highlighting the remarkable IL‐17 action in the initiation and, more importantly, the development of vitiligo 55,91 …”

“…Studies have reported a correlation between the extent of depigmentation and increased level of IL‐17 in sera or lesion biopsy in vitiligo patients 55,92–94 ; as well as the existence of IL‐17 genotype 95,96 …”

“…It is considered as a known trigger of various autoimmune disorders including psoriasis, rheumatoid arthritis, and multiple sclerosis. 90,91 Studies have reported a correlation between the extent of depigmentation and increased level of IL-17 in sera or lesion biopsy in vitiligo patients 55, [92][93][94] ; as well as the existence of IL-17 genotype. 95,96 IL-17 affects melanocytes by the two proposed mechanisms:…”