Effect of interleukin-12 gene expression on insulin resistance in patients with acne vulgaris.

BACKGROUND: Insulin resistance (IR) is a condition where cells become resistant to insulin, causing impaired glucose uptake and increased blood glucose levels. Interleukin-12 (IL-12), a cytokine, regulates the immune system. High levels of IL-12 can lead to chronic inflammation, exacerbate resistance to insulin, and contribute to type 2 diabetes. Also, link IR to acne vulgaris (AV), as it reduces tissue sensitivity to insulin, causing increased insulin levels and sebum production, which can contribute to acne development. AIM: To explore the role of IL-12 gene expression on IR in AV patients and to study the role of IL-12 gene in the development of AV. SUBJECTS AND METHODS: A case-control study was performed on 68 AV patients and 68 healthy controls. The biochemical analysis included fasting glucose, fasting insulin, (HOMA-IR), and serum IL-12 level. IL-12 gene expression was performed by quantitative real-time PCR for both two groups. In addition, folding change was calculated by using the standard 2-(∆∆Ct) method. RESULT: IL-12 level, IL-12 folding change, fasting insulin, and IR were all increased in acne patients. A highly significant linear correlation was found between IL-12 folding change and both IL-12 levels and IR. There is a substantial positive significant simple linear association between IL-12 level and IL-12 folding change, as well as IR and IL-12 folding change, in moderate and severe acne. CONCLUSION: IL-12 gene has an important role in IR and the development of acne in AV patients.

MicroRNA-17-92a-1 Host Gene (MIR17HG) Expression Signature and rs4284505 Variant Association with Alopecia Areata: A Case-Control Study.

Accumulating evidence indicates the implication of microRNAs (miRs) in cutaneous and hair follicle immunobiology. We evaluated, for the first time, the miR-17-92a-1 cluster host gene (MIR17HG) expression in peripheral blood of 248 unrelated alopecia areata (AA) patients compared to 244 matched controls using Real-Time qPCR. We also tested its association with different rs4284505A>G genotypes (based on TaqMan allelic discrimination PCR) and the available clinical data. The adjusted odds ratio (OR) and 95% confidence interval (CI) were calculated for each genetic association model. The upregulation of miR-17 was observed in the serum of patients with alopecia compared to controls (p-value = 0.004). The ROC curve showed high diagnostic performance of miR-17 in differentiating between patients and controls (AUC = 0.85, p-value < 0.001). rs4284505*A/G heterozygotes were more susceptible to the disease (OR = 1.57, 95% CI = 1.01−2.45) under the over-dominant model. Interestingly, patients with the rs4284505*G/G genotype had a higher level of miR-17 than those with the A/A and A/G genotypes. The G/G genotype was associated with the severe phenotype (p-value = 0.038). A/G carriers were the youngest (p-value < 0.001), had more frequent scalp infection (p-value = 0.006), exhibited the worst dermatology life quality index score (p-value = 0.037), and responded less to treatment (p-value = 0.033). In conclusion, MIR17HG expression and the rs4284505 variant were significantly associated with AA and could play a role in pathogenesis and phenotype in the Egyptian population. Further multi-center studies in other ethnicities are warranted to replicate the findings.

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

Background: Alopecia areata (AA) is an acquired hair loss disorder induced by a cell-mediated autoimmune attack against anagen hair follicles. CD27-CD70 is a receptor-ligand complex which enhances T helper and cytotoxic T cell activation, survival, and proliferation. The overstimulation of this complex can lead to a lack of tolerance and the development of autoimmunity. Objectives: This study aimed to assess the gene expression of CD27 and CD70 in patients with AA. Methods: CD70 and CD27 mRNA expressions were evaluated by a quantitative real-time polymerase chain reaction in scalp biopsies from 40 AA patients (both AA lesions and non-lesional areas) and 40 healthy controls (HCs). The Severity of Alopecia Tool (SALT) score was used to assess AA severity. Patients were evaluated for signs of AA activity, including a positive hair pull test and dermoscopic features of black dots, broken hairs, and tapering hairs. Results: The gene expression of CD70 and CD27 was significantly higher in AA lesions than in non-lesional areas (p < 0.001 for both) and HCs (p=0.004, p=0.014, respectively). There were significant positive correlations between AA severity and gene expression of CD70 (p < 0.001) and CD27 (p=0.030) in AA lesions. Significant associations were detected between signs of AA activity and lesional gene expression of CD70 and CD27. Additionally, CD70 and CD27 gene expression was significantly lower in non-lesional biopsies compared to HCs (p < 0.001). Conclusion: Gene expression of CD70 and CD27 was increased in AA lesions and was associated with disease severity and activity. Thus, both molecules can be a predictor of AA severity and activity. Furthermore, the expression was reduced in non-lesional scalp areas. Thus, a lack of CD27 and CD70 expression may initially predispose to immunological dysregulation and the development of AA.

Serum level of interleukin-22 in patients with cutaneous warts: A case-control study.

BACKGROUND: Warts are viral cutaneous infections caused by human papilloma virus (HPV), presented by verrucous growth over the skin surface. The immune response is considered to play a crucial role in HPV clearance. It depends on intact cellular immunity including natural killer (NK) cell and cytotoxic T cells. It has been clarified that T-helper (Th) 1 cytokines (interleukin (IL)-2, interferon-γ, and tumor necrosis factor-a) and IL-17 are involved in HPV clearance. IL-22 is one of IL-10 family of cytokines produced by NK cells, Th1, Th17, and Th22 cells. In the skin, IL-22 reduces keratinocyte cornification and enhances keratinocyte production of antimicrobial peptides. IL-22 overexpression has been demonstrated in various viral infections and skin inflammatory disorders. AIM: The aim of this study was to assess serum levels of IL-22 in patients with warts and its association with their different clinical characteristics. METHODS: The study included 20 patients with warts and 20 control subjects. Serum concentration of IL-22 was measured by enzyme-linked immune sorbent assay. RESULTS: Serum levels of IL-22 were significantly higher in patients with warts than in control subjects (P < .001). The levels were significantly higher in patients with recurrent warts after prior treatment than in patients with first-time warts (P = .007). Moreover, a significant positive correlation was detected between serum levels of IL-22 and the number of warts (P = .017). CONCLUSION: Serum level of IL-22 was elevated in patients with warts. Thus, IL-22 may have a crucial role in the antiviral immune response against this infection.

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

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.