Expression of survivin and p53 genes in patients with alopecia areata: A case–control study

Abstract

Background Alopecia areata is a common non‐scarring hair loss disorder. It has been generally recognised as a loss of immune privilege leading to an autoimmune attack upon anagen hair follicles. Survivin is one of the apoptosis inhibitor proteins, responsible for apoptosis suppression and cell cycle regulation. Survivin expression has been demonstrated in the matrix and outer root sheath keratinocytes of anagen hair follicles. Survivin overexpression was shown in several autoimmune diseases, and it was postulated that it contributes to the survival of self‐reactive T and B cells. P53 is a tumour suppressor gene that was suggested to repress autoimmunity via induction of T regulatory cells. Survivin gene expression is transcriptionally suppressed by wild‐type p53. Aim The aim of this study was to investigate survivin and p53 genes expression in alopecia areata patients. Methods The mRNA tissue expression of survivin and p53 was measured by quantitative real‐time polymerase chain reaction in lesional and non‐lesional punch scalp biopsies of 25 alopecia areata patients and 25 healthy subjects. Results The study showed higher mRNA expression of survivin in lesional biopsies compared to non‐lesional (P < 0.001) and control biopsies (P = 0.001). In non‐lesional biopsies, the expression was significantly lower than in control biopsies (P < 0.001). The expression of p53 was lower in both lesional and non‐lesional biopsies relative to control biopsies. However, the difference was only significant in non‐lesional biopsies (P = 0.017). Conclusion Our results suggested that survivin and p53 genes expression was altered in patients with alopecia areata.

The alterations of gene expression of interleukin‐36α and interleukin‐37 between alopecia areata patients and healthy controls

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relatively short follow-up, the low sample size and the long-lasting response to the adalimumab originator at the time of the shift for many patients, the results are in line with previous comparability studies 1,3,4,5 and demonstrate that the biosimilar adalimumab has shown not to be less effective than the originator and the transition to biosimilar adalimumab in psoriasis patients treated with the originator is a safe and effective choice in a real-life setting of moderate to severe psoriasis patients as previously observed in other biologic treatments, in particular infliximab. 6 The only difference we observed was a significant worsening of the assessment of pain in a subpopulation of patients with BMI> 25 between T0 and T1 suggesting the need of further evaluations and objective data, also with a multi-specialist team.

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“…It is widely claimed as an autoimmune assault against the anagen hair follicles in which T-helper 1 (Th) and Th17 are implicated. 1 IL-36a promotes Th1 and Th17 polarisation, 2 whereas IL-37 represses Th1 and Th17 immune Letter To The Editors responses. 3 The altered expressions of IL-36a and IL-37 were demonstrated in several autoimmune diseases but were poorly investigated in AA.…”

“…Alopecia areata (AA) is a common, non‐scarring hair loss. It is widely claimed as an autoimmune assault against the anagen hair follicles in which T‐helper 1 (Th) and Th17 are implicated 1 . IL‐36α promotes Th1 and Th17 polarisation, 2 whereas IL‐37 represses Th1 and Th17 immune responses 3 .…”

“…Cutaneous adverse effects (cAEs) are a frequently reported toxicity of PD-1 inhibitors, occurring in up to 49% of patients. 1 Various cAEs have been described including lichenoid reactions, eczema, vitiligo, immunobullous conditions, eruptive maculopapular rash, keratoacanthoma and squamous cell carcinoma. [1][2][3][4][5] We report a case of a patient who ironically developed eruptive Bowen's disease while on pembrolizumab for Hodgkin's lymphoma, despite the fact pembrolizumab is known to treat locally advanced and metastatic SCCs.…”

Gene Expression of CD70 and CD27 Is Increased in Alopecia Areata Lesions and Associated with Disease Severity and Activity

“…Alopecia areata (AA) is an acquired non-cicatricial hair loss disorder affecting 0.1%–0.2% of individuals worldwide [ 1 ]. A collapse of the hair follicle (HF) immune privilege causing a CD8+ cytotoxic T (cT) cell assault against anagen HFs is implicated in AA development [ 2 , 3 ]. However, the precise molecular mechanisms are still poorly established.…”