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This randomized, observer-blinded, intrapatient comparative study sought to investigate the efficacy and safety of TCA 35% vs. 5-aminolaevulinic acid (ALA) 20% photodynamic therapy (PDT) in patients with extensive field cancerization and multiple AKs. Twenty-eight patients with at least five AKs in two comparable anatomical areas on the head were treated with TCA 35% and ALA PDT randomly assigned to each area. Their therapeutic efficacy, adverse events and cosmetic outcome were assessed by a blinded investigator at 1, 3, 6 and 12 months after treatment.
The choice for a profession in general and for MDs in particular regarding the decision to concentrate on a certain discipline is almost never straightforward and often entails a high degree of serendipity.
Editorial note: Welcome to the Journal of Investigative Dermatology (JID) Cells to Surgery Quiz— In this monthly online-only quiz, the first question (“What is your diagnosis?”) relates to the clinical image above, while additional questions concern the findings reported in a JID article that provides new information about that disease entity.
Editorial note: Welcome to the Journal of Investigative Dermatology (JID) Snapshot Dx Quiz— In this monthly online-only quiz, the first question (“What is your diagnosis?”) relates to the clinical image above, while additional questions concern the findings reported in a JID article that provides new information about that disease entity.
Dendritic cell (DC) subsets historically have been defined on the basis of morphology, physical properties, localization, molecular markers, and function. In an effort to better assess the diversity of blood DCs and monocytes without bias, Villani and colleagues used deep sequencing at the single cell level (scRNA-seq) to classify these cells from a single healthy individual. These studies identified six DC populations, including further division of previously designated DC populations and a subpopulation that forms the continuum between plasmatoid DCs and CD1C+ DCs.
Previous reports have established a fundamental relationship between sebum reduction and acne improvement. After identifying the fatty acid biosynthesis enzyme acetyl coenzyme A carboxylase (ACC) in sebaceous glands, Hunt and colleagues demonstrated that application of the ACC inhibitor olumacostat glasaretil (OG) suppressed de novo lipid synthesis in human sebocytes in culture and reduced hamster ear sebaceous gland size. Thus, in accord with recent clinical trials, these results support the well-tolerated targeting of ACC for suppression of sebaceous gland activity to reduce sebum, an important factor in acne pathogenesis.
Maintenance of hair follicle (HF) stem cell quiescence and self-renewal are key functions of a specific cellular niche represented by the HF bulge and adjacent cell populations. The unique context of this niche is crucial for normal HF functioning, but mechanisms implicated in its maintenance are still not quite clear. The Letter to the Editor by Sada et al. introduces a novel Slc1a3-CreER genetic mouse model which, in contrast to previously reported marking tools, selectively and highly efficiently demarcates the telogen bulge inner layer, one of the critical structural components of the bulge stem cell niche.
Vitiligo, the most common depigmenting disorder, is caused by immune destruction of melanocytes by cytotoxic CD8+ T cells. One weakness in vitiligo management is the lack of an assessment method for active depigmentation. Beginning with reports about increased S100B levels in different inflammatory and tissue damage processes, Speeckaert et al. explored correlations between the S100B dynamics and vitiligo activity, identifying high circulating S100B levels in patients with active depigmentation which were strongly correlated with the extent of affected skin surface.
The 65th annual Montagna Symposium on the Biology of the Skin, “The Skin: Our Sensory Organ for Itch, Pain, Touch and Pleasure,” was held October 20–24, 2016, in Gleneden Beach, Oregon, USA. Gil Yosipovitch (University of Miami, Florida) served as Program Chair, with Ethan Lerner (Harvard Medical School/Massachusetts General Hospital, Boston), Diana Bautista (University of California, Berkeley, California), Ellen A. Lumpkin (Columbia University, New York, New York), and Francis McGlone (Liverpool John Moores University, UK) serving as Session Chairs.
Cost-effectiveness analysis (CEA) is a research method used to determine the clinical benefit-to-cost ratio of a given intervention. CEA offers a standardized means of comparing cost-effectiveness among interventions. Changes in quality-adjusted life-years, disability-adjusted life-years, or survival and mortality are some of the common clinical benefit measures incorporated into CEA. Because accounting for all associated costs and benefits of an intervention is complex and potentially introduces uncertainty into the analysis, sensitivity analyses can be performed to test the analytic model under varying conditions.
Hunt et al. show that olumacostat glasaretil, an inhibitor of acetyl coenzyme A carboxylase, reduces saturated and monounsaturated fatty acyl chains in sebaceous lipids. Topical olumacostat glasaretil application decreases hamster ear sebaceous gland size and shows efficacy in treating patients with acne vulgaris. Olumacostat glasaretil-mediated sebum suppression may reduce Propionibacterium acnes growth and biofilm formation, comedogenesis, and inflammation.
Pemphigus is a skin and mucosal membrane-targeting autoimmune bullous disease. Previous studies have demonstrated that circulating anti-desmoglein1/3 antibodies are pathogenic and mediate blister formation. However, the role of infiltrated immune cells in the lesional skin has not been fully investigated. In this study we showed that there existed a large number of B, T lymphocytes and plasma cells in the skin lesions by immunohistochemistry and immunofluorescence staining. In addition, a significantly increased number of Dsg1 and Dsg3-specific B cells could be identified by flow cytometric analysis or ELISPOT assay.
Inhibitor of Apoptosis Proteins (IAPs) are critical regulators of cell death and survival pathways. Mice lacking cellular IAP (cIAP) 1 and either cIAP2 or X-linked IAP (XIAP) die in utero, and myeloid lineage-specific deletion of all IAPs causes sterile inflammation, but their role in the skin is unknown. We generated epidermal-specific IAPs deficient mice and found that combined genetic deletion of cIAP1 in keratinocytes and ubiquitous cIAP2 deletion (cIap1EKO/EKO.cIap2-/-) caused profound skin inflammation and keratinocyte death, lethal by post-partum day 10.
On acquisition of an oncogenic mutation, primary human and mouse cells can enter oncogene-induced senescence (OIS). OIS is characterized by a stable proliferation arrest and secretion of pro-inflammatory cytokines and chemokines, the senescence-associated secretory phenotype (SASP). Proliferation arrest and the SASP collaborate to enact tumor suppression, the former by blocking cell proliferation and the latter by recruiting immune cells to clear damaged cells. However, the interactions of OIS cells with the immune system are still poorly defined.
The skin microbiome exists in dynamic equilibrium with the host but when the skin is compromised, bacteria can colonise the wound and impair wound healing. Thus the interplay between normal skin-microbial interactions versus pathogenic-microbial interactions in wound repair is important. Bacteria are recognised by innate host pattern recognition receptors (PRRs) and we previously demonstrated an important role for the PRR NOD2 (nucleotide-binding oligomerisation domains-containing protein 2) in skin wound repair.
Varicella Zoster Virus (VZV) is a human-restricted α-herpesvirus that exhibits tropism for the skin. The VZV host receptors and downstream signaling pathways responsible for the antiviral innate immune response in the skin are not completely understood. Here, we show that stimulator of interferon genes (STING) mediates an important host defense against VZV infection in dermal cells including human dermal fibroblasts (HDFs) and HaCaT keratinocytes. Inhibition of STING using small interfering RNA (siRNA) or short hairpin RNA (shRNA)-mediated gene disruption resulted in enhanced viral replication but diminished IRF3 phosphorylation and induction of IFNs and pro-inflammatory cytokines.
All Leishmania spp. parasites are introduced into mammalian skin through a sand fly bite, but different species cause distinct clinical outcomes. Mouse studies suggest early responses are critical determinants of subsequent adaptive immunity in leishmaniasis, yet few studies address the role of keratinocytes, the most abundant cell in the epidermis. We hypothesized Leishmania infection causes keratinocytes to produce immunomodulatory factors that influence the outcome of infection. Incubation of primary or immortalized human keratinocytes with Leishmania infantum or Leishmania major, which cause visceral or cutaneous leishmaniasis, respectively, elicited dramatically different responses.