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It is unclear to what degree genomic and traditional (phenotypic and environmental) risk factors overlap in their prediction of melanoma risk. We evaluated the incremental contribution of common genomic variants (in pigmentation, nevus and other pathways) and their overlap with traditional risk factors, using data from two population-based case-control studies from Australia (n=1,035) and the UK (n=1,460) that used the same questionnaires. Polygenic risk scores were derived from 21 gene regions associated with melanoma and odds ratios from published meta-analyses.
Destruction of epidermal barrier function associated with atopic dermatitis or Darier's disease often causes severe secondary skin infections. Patients with skin barrier disorders often repeatedly acquire Kaposi varicelliform eruption, which is caused by herpes simplex virus, but the underlying mechanisms and effective preventive methods have yet to be found. Viral infection through an impaired epidermal barrier can be prevented by enhancing innate immunity and/or inhibiting viral entry. In this study, we established a three-dimensional skin barrier dysfunction model by silencing ATP2A2, which is mutated in some Darier's disease patients.
Psoriasis is a chronic inflammatory skin disease dependent on the IL-23/IL-17 axis, a potent inflammatory pathway involved in pathogen clearance and autoimmunity. Several triggers have been proposed as initiators for psoriasis, including alarmins such as ATP. However, the role of alarmins in psoriasis pathogenesis and cutaneous inflammation has not been well addressed. Herein studies demonstrate that signaling through the P2X7 receptor (P2X7R) pathway underlies the development of psoriasiform inflammation.
Ingram and colleagues from Cardiff explain that epidemiology data regarding hidradenitis suppurativa (HS) are conflicting, and prevalence estimates vary 80-fold, from 0.05% in a population-based study to 4%. The aim of this study was to assess the hypothesis that previous population-based studies underestimated true HS prevalence by missing undiagnosed cases. A population-based observational and case–control study was performed using the U.K. Clinical Practice Research Datalink (CPRD) linked to hospital episode statistics data.
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) SnapshotDx Quiz. In this monthly online-only quiz, the first question relates to the clinical image found above, while additional questions concern the findings reported in a JID article that provides new information about that disease entity.
Indoleamine 2,3-Dioxygenase Expression in Primary Cutaneous Melanoma Correlates with Breslow Thickness and Is of Significant Prognostic Value for Progression-Free Survival
For decades, the nociceptive neurons that convey pain have been known, but the molecular mechanisms involved in detecting noxious thermal and mechanical signals have yet to be elucidated. Previous studies indicated the transient receptor potential (TRP) ion channel TRPV1 is involved in responses to these signals, but because loss of this protein results in only minor deficits in acute noxious heat sensing, other players are also involved. Vandewauw and colleagues demonstrated that TRPA1, TRPV1, and TRPM3 play critical and redundant roles in heat signal transduction, as indicated by the fact that triple knockout or inhibition of all three channels resulted in the nearly complete loss of heat responses in mice without concomitant defects in other sensory neuron biology features.
The pathogenesis of generalized pustular psoriasis (GPP), a rare, highly inflammatory psoriasis variant, is incompletely understood. Recent success with cyclosporine or CD4+ T cell modulators in GPP suggests that T cells are integral to disease pathogenesis. Arakawa and colleagues found that GPP involves antigen-driven T helper 17 responses that, in the context of certain HLA-class II alleles, are facilitated by unopposed interleukin (IL)-36 signaling, which promotes CD4+ T cell responses. CD4+ T cells were highly proliferative and produced high levels of IL-17A in blood and skin lesions.
Cell Surface Expression of HLA-Cw6 by Human Epidermal Keratinocytes: Positive Regulation by Cytokines, Lack of Correlation to a Variant Upstream of HLA-C
The phenomenon of wound-induced hair neogenesis in adult mice and rabbits offers a tantalizing window into the mechanisms of regeneration. By comparing wounds in mice and several rat strains, Guerrero-Juarez et al. attempted to identify factors that may contribute to the failure of wound-induced hair neogenesis to occur in the rat. In addition to biochemical, cellular, and molecular variation, worthwhile comparisons could include the magnitude, distribution, and source of tensional forces within the wound environment.
Bullous pemphigoid is an autoantibody-mediated skin blistering disease. Previous studies revealed that intravenous Ig is therapeutic in animal models of bullous pemphigoid by saturating the IgG-protective receptor FcRn, thereby accelerating degradation of pathogenic IgG. Sasaoka et al. demonstrate that the inhibitory effects of intravenous Ig on bullous pemphigoid are also associated with negative modulation of cytokine production by keratinocytes.