Abstract
Alopecia areata is a type of non-scarring hair loss. The dysregulation of numerous systemic Th1 (IL-2, IFN-γ, TNF, IL-12, and IL-18), Th2 (IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, IL-17E, IL-31 and IL-33) and Th17 (IL-17, IL-17F, IL-21, IL-22, IL-23 and TGF-β) cytokines was observed in patients with alopecia areata. Positive correlations between the severity of alopecia areata and an increased serum level of various cytokines including IL-2, TNF, IL-12, IL-17, and IL-17E were reported in the literature. An increased serum level of numerous cytokines, such as IL-2, IL-6, TNF, IL-12, IL-17E, and IL-22, was described as positively correlated with the duration of the disease. Moreover, it was shown that increased pre-treatment serum level of IL-12 was a positive, while increased serum levels of IL-4 and IL-13 were negative prognostic markers for the efficacy of diphenylcyclopropenone. In conclusion, alopecia areata is associated with the dysregulation of systemic Th1, Th2 and Th17 cytokines with their role in the pathogenesis, clinical manifestations and prognosis of the disease. Available data indicate the most significant role of serum IL-2, TNF, IL-12, IL-17, and IL-17E as markers of disease activity. The serum levels IL-4, IL-12 and IL-13 may be useful as potential predictors of diphenylcyclopropenone efficacy.
Highlights
Studies conducted by Bain et al [49] and Atwa et al [47] demonstrated an increased serum level of Interleukin 21 (IL-21) in patients with alopecia areata compared to healthy controls
It was reported that the local dysregulation of T helper 1 (Th1), T helper 2 (Th2) and T helper 17 (Th17) cytokine secretion played an important role in the pathogenesis of alopecia areata [8,19]
Alopecia areata is characterized by systemic dysregulation of Th1
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Contact immunotherapy with diphenylcyclopropenone (DPCP) and squaric acid dibutylester (SADBE) is mainly recommended for limited hair loss [7] By some authors, it is considered as first-line therapy in children with alopecia areata. In the case of the insufficient activity of immunosuppressive molecules, proinflammatory cytokines including substance P and Interferon-gamma (IFN-γ) induce the ectopic expression of MHC class antigens and the over-expression of adhesion molecules in hair follicle keratinocytes and dermal papilla cells [13]. It results in activation of the cytotoxic, CD8+ T cell pathway and increased migration of antigen presenting cells to the area. The clinical role of serum Th1, Th2, and Th17 cytokines in patients with alopecia areata is discussed in this review
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