Background Vitiligo is a common acquired disorder of depigmentation. Its pathogenesis entails a T helper (Th) 1‐cytotoxic T (cT) lymphocytes mediated autoimmune melanocyte destruction. Interleukin (IL)‐15 is one of the IL‐2 family of cytokines and shares several actions with IL‐2. IL‐15 enhances survival, maturation, and functional activity of natural killer, neutrophils, and dendritic cells. Furthermore, it potentiates survival, maturation, and cytotoxicity of memory cT cells. IL‐15 has been shown to play a crucial role in the pathogenesis of several autoimmune diseases but was poorly investigated in patients with vitiligo. Aims The study aimed at evaluating IL‐15 level in the sera of patients with vitiligo and its association with vitiligo severity and activity. Patients and Methods The study included 30 patients with nonsegmental vitiligo and 30 healthy controls. Vitiligo Extent Score (VES) and Vitiligo Disease Activity (VIDA) score were used to assess vitiligo severity and activity, respectively. Serum level of IL‐15 was assessed by enzyme‐linked immune‐sorbent assay. Results Serum IL‐15 level, in patients with vitiligo, was significantly higher in comparison with the control group (P = .001). A significant positive correlation was found between serum IL‐15 level and VES score (P = .001), whereas there was no significant correlation between IL‐15 level and VIDA score as well as the disease duration. Conclusion IL‐15 level was elevated in the sera of patients with vitiligo. IL‐15 may therefore have a significant impact on vitiligo autoimmune pathogenesis, and further identification of its molecular roles may highlight new therapeutic strategies for vitiligo.

Alopecia areata (AA) is a recurrent, immune-mediated, hair-loss disorder. It is associated with other autoimmune disorders that carry a high risk of cardiovascular disease (CVD). However, there is a lack of reports on the association of cardiovascular comorbidities and AA. Cardiac troponin I is a biomarker of myocardial ischaemia and inflammation, while N-terminal pro-B-type natriuretic peptide is used in the diagnosis of congestive heart failure. This study was conducted to assess the serum level of both markers by ELISA in 44 patients with AA compared with 44 healthy controls (HCs). None of the participants had CVD, CVD risk factors or other diseases associated with elevation of either marker. The study revealed that serum levels of both markers were significantly higher in patients with AA compared with HCs (P < 0.001). The inflammatory milieu encountered in AA may be associated with subtle myocardial inflammation that causes elevation of levels of both of these cardiac markers.

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.

Background Vitiligo is an acquired cutaneous depigmenting disease caused by a T helper (Th) 1–cytotoxic T cells driven autoimmune attack against melanocytes, in which Th17 is also involved. Interleukin (IL)‐38 belongs to the IL‐1 family of cytokines and suppresses Th1 and Th17 activation. IL‐38 protein and mRNA levels have been found to be elevated in various autoimmune disorders and correlated with disease severity and activity, including psoriasis, systemic sclerosis, rheumatoid arthritis, and atopic dermatitis. No previous studies have been performed to investigate the expression of IL‐38 in patients with vitiligo. Aim To evaluate IL‐38 serum level in patients with vitiligo compared to healthy controls (Hcs) and examine the association between IL‐38 level and severity and activity of vitiligo. Patients and Methods The study comprised 21 patients with vitiligo and 21 Hcs. Vitiligo severity and activity were evaluated via Vitiligo Extent Score (VES) and Vitiligo Disease Activity (VIDA) Score, respectively. IL‐38 serum level was evaluated by enzyme‐linked immunosorbent assay. Results Vitiligo patients had significantly higher serum level of IL‐38 than Hcs (p < 0.001). This level was significantly higher among patients with signs of vitiligo activity (p = 0.048), correlated positively with VES (p < 0.001), and correlated negatively with the age of patients (p = 0.001) and the age of disease onset (p = 0.022). Conclusion IL‐38 serum level was higher in patients with vitiligo than in Hcs and was related to vitiligo severity and signs of activity.

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