The mechanisms of inflammation in acne are currently subject of intense investigation. This study focused on the activation of adaptive and innate immunity in clinically early visible inflamed acne lesions and was performed in two independent patient populations. Biopsies were collected from lesional and non-lesional skin of acne patients. Using Affymetrix Genechips, we observed significant elevation of the signature cytokines of the Th17 lineage in acne lesions compared to non-lesional skin. The increased expression of IL-17 was confirmed at the RNA and also protein level with real-time PCR (RT-PCR) and Luminex technology. Cytokines involved in Th17 lineage differentiation (IL-1β, IL-6, TGF-β, IL23p19) were remarkably induced at the RNA level. In addition, proinflammatory cytokines and chemokines (TNF-α, IL-8, CSF2 and CCL20), Th1 markers (IL12p40, CXCR3, T-bet, IFN-γ), T regulatory cell markers (Foxp3, IL-10, TGF-β) and IL-17 related antimicrobial peptides (S100A7, S100A9, lipocalin, hBD2, hBD3, hCAP18) were induced. Importantly, immunohistochemistry revealed significantly increased numbers of IL-17A positive T cells and CD83 dendritic cells in the acne lesions. In summary our results demonstrate the presence of IL-17A positive T cells and the activation of Th17-related cytokines in acne lesions, indicating that the Th17 pathway is activated and may play a pivotal role in the disease process, possibly offering new targets of therapy.

Vitiligo affects 1% of the worldwide population. Halting disease progression and repigmenting the lesional skin represent the two faces of therapeutic challenge in vitiligo. We performed transcriptome analysis on lesional, perilesional, and non-depigmented skin from vitiligo patients and on matched skin from healthy subjects. We found a significant increase in CXCL10 in non-depigmented and perilesional vitiligo skin compared with levels in healthy control skin; however, neither CXCL10 nor other immune factors were deregulated in depigmented vitiligo skin. Interestingly, the WNT pathway, which is involved in melanocyte differentiation, was altered specifically in vitiligo skin. We demonstrated that oxidative stress decreases WNT expression/activation in keratinocytes and melanocytes. We developed an ex vivo skin model and confirmed the decrease activation of the WNT pathway in human skin subjected to oxidative stress. Finally, using pharmacological agents that activate the WNT pathway, we treated ex vivo depigmented skin from vitiligo patients and successfully induced differentiation of resident stem cells into pre-melanocytes. Our results shed light on the previously unrecognized role of decreased WNT activation in the prevention of melanocyte differentiation in depigmented vitiligo skin. Furthermore, these results support further clinical exploration of WNT agonists to repigment vitiligo lesions.

Background Severe nodular acne is characterized by inflammatory nodules and scarring. Their natural evolution and duration are insufficiently investigated. Aim To investigate the evolution and duration of untreated acne nodules. Methodology Four‐week, single‐centre, non‐interventional, prospective study in subjects with severe nodular acne on the back. Nodule evolution and duration was assessed using standardized photographs taken twice weekly. Results Data from 23 subjects were evaluable. Mean age was 25.1 ± 4.9 years, 87% were males, and mean acne duration was 9.7 ± 6.7 years. At baseline, the overall total nodule count was 132 (mean number: 5.7 ± 3.0 nodules/subject). Among others, the following two main pathways were observed: nodules evolving directly into atrophic scars (31.8%) and nodules evolving towards papules into atrophic scars (37.9%). After 4 weeks, 77.3% of baseline nodules had evolved into atrophic scars. After baseline visit, a total of 247 new nodules (3.1 ± 2.2 nodules/week/subject) with a mean duration of 4.9 ± 2.6 days were observed. The mean duration of new nodules was significantly longer in subjects (n = 16) with ≥6 new nodules compared to subjects (n = 7) with <6 new nodules (5.2 ± 1.4 vs. 3.6 ± 0.8 days; P = 0.008)). There was no correlation between the number of new nodules and acne duration or with the number of baseline nodules. Conclusion This study documents the natural nodule evolution and duration over 4 weeks and showed in 23 patients the scarring potential of untreated severe nodular acne of the back.