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    Interleukin-17RA blockade by brodalumab decreases inflammatory pathways in hidradenitis suppurativa skin and serum. The British journal of dermatology 10.1111/bjd.21591
    miR-378a: an amplifier of the interleukin-17A response in keratinocytes. The British journal of dermatology 10.1111/bjd.21592
    Biomarkers of disease progression in people with psoriasis: a scoping review. The British journal of dermatology BACKGROUND:Identification of those at risk of more severe psoriasis and/or associated morbidities offers opportunity for early intervention, reduced disease burden and more cost-effective healthcare. Prognostic biomarkers of disease progression have thus been the focus of intense research, but none are part of routine practice. OBJECTIVES:To identify and catalogue candidate biomarkers of disease progression in psoriasis for the translational research community. METHODS:A systematic search of CENTRAL, Embase, LILACS, and MEDLINE was performed for relevant articles published between 1990 and December 2021. Eligibility criteria were studies involving the psoriasis population (any age, n ≥50) reporting biomarkers associated with disease progression. The main outcomes were any measure of skin severity or any pre-specified psoriasis comorbidity. Data were extracted by one reviewer and checked by a second; studies meeting minimal quality criteria (longitudinal design and/or use of methods to control for confounding) were formally assessed for bias. Candidate biomarkers were identified by an expert multi-stakeholder group using a majority voting consensus exercise, and mapped to relevant cellular and molecular pathways. RESULTS:Of 181 included studies, most investigated genomic or proteomic biomarkers associated with disease severity (n=145) or psoriatic arthritis (n=30). Methodological and reporting limitations compromised interpretation of findings, most notably a lack of longitudinal studies, and inadequate control for key prognostic factors. Candidate biomarkers with future potential utility were identified for predicting disease severity: LCE3D, IL23R, IL23A, NFKBIL1 loci, HLA-C*06:02 (genomic), IL-17A, IgG aHDL, GlycA, I-FABP and Kallikrein 8 (proteomic), tyramine (metabolomic); PsA: HLA-C*06:02, HLA-B*27, HLA-B*38, HLA-B*08, and variation at the IL23R and IL13 loci (genomic); IL-17A, CXCL10, Mac-2 binding protein, Integrin b5, MMP-3 and M-CSF(proteomic) and tyramine and mucic acid (metabolomic) and type 2 diabetes mellitus: variation in IL12B and IL23R loci (genomic). No biomarkers were supported by sufficient evidence for clinical use without further validation. CONCLUSIONS:This review provides a comprehensive catalogue of investigated biomarkers of disease progression in psoriasis. Future studies must address the common methodological limitations identified here to expedite discovery and validation of biomarkers for clinical use. 10.1111/bjd.21627
    The biological basis of disease recurrence in psoriasis: a historical perspective and current models. The British journal of dermatology A key challenge in psoriasis therapy is the tendency for lesions to recur in previously affected anatomical locations after treatment discontinuation following lesion resolution. Available evidence supports the concept of a localized immunological 'memory' that persists in resolved skin after complete disappearance of visible inflammation, as well as the role of a specific subpopulation of T cells characterized by the dermotropic CCR4 phenotype and forming a local memory. Increasing knowledge of the interleukin (IL)-23/T helper 17 (Th17) cell pathway in psoriasis immunopathology is pointing away from the historical classification of psoriasis as primarily a Th1-type disease. Research undertaken from the 1990s to the mid-2000s provided evidence for the existence of a large population of CD8 and CD4 tissue-resident memory T cells in resolved skin, which can initiate and perpetuate immune responses of psoriasis in the absence of T-cell recruitment from the blood. Dendritic cells (DCs) are antigen-presenting cells that contribute to psoriasis pathology via the secretion of IL-23, the upstream regulator of Th17 cells, while plasmacytoid DCs are involved via IL-36 signalling and type I interferon activation. Overall, the evidence discussed in this review indicates that IL-23-driven/IL-17-producing T cells play a critical role in psoriasis pathology and recurrence, making these cytokines logical therapeutic targets. The review also explains the clinical efficacy of IL-17 and IL-23 receptor blockers in the treatment of psoriasis. 10.1111/bjd.20963
    Topical application of lipids to correct abnormalities in the epidermal lipid barrier. The British journal of dermatology 10.1111/bjd.21294
    Polygenic risk scores for melanoma: a stepwise process towards clinical implementation. The British journal of dermatology 10.1111/bjd.21296
    Does acral melanoma need a distinctive prognostic staging system? The British journal of dermatology 10.1111/bjd.21585
    The effect of screening on melanoma incidence and biopsy rates. The British journal of dermatology BACKGROUND:Cutaneous melanomas are common cancers in white populations and early detection is promoted as a means of reducing morbidity and mortality. There is concern that increased skin screening is leading to overdiagnosis of indolent melanomas with low risk of lethality. The extent of melanoma overdiagnosis associated with screening is unknown. OBJECTIVE:We sought to estimate possible overdiagnosis by comparing subsequent melanoma incidence and biopsy rates among people subjected to skin screening with those who were not. METHODS:We recruited 43,762 residents of Queensland, Australia aged 40-69 years with no prior history of melanoma, selected at random from a population register in 2010. At baseline, participants completed a comprehensive melanoma risk factor survey, and were asked if their skin had been examined by a doctor in the 3 years prior to baseline. We calculated incidence and relative risk of histologically confirmed melanoma (invasive and in situ) in years 2 to 7 of follow-up, obtained through linkage to the cancer registry. In secondary analyses, we measured biopsy rates in years 2 to 6 of follow-up. We used propensity score analysis to calculate adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs). RESULTS:28,155 (73%) participants underwent skin screening prior to baseline. We observed 967 first incident melanomas (381 invasive) during 197,191 person-years of follow-up. Those screened had higher rates of melanoma (aHR 1.29, 95% CI 1.02-1.63) and subsequent skin biopses (aHR 1.85, 95% CI 1.69-2.04) than unscreened participants. The higher risk associated with skin screening was evident for in situ melanoma (aHR 1.45, 95% CI 1.09-1.92) but not invasive melanoma (aHR 1.05, 95% CI 0.72-1.54). In secondary analyses where screening was defined as having a skin biopsy in the first year after baseline, we observed significantly increased risks of melanoma (adjusted aHR 1.53, 95%CI 1.23-1.89) and subsequent biopsies (aHR 2.64, 95% CI 2.46-2.84) relative to those who did not have a biopsy. CONCLUSIONS:People who undergo skin screening subsequently experience higher rates of biopsies and melanoma (especially in situ melanoma), even after adjusting for all known risk factors, consistent with overdiagnosis. 10.1111/bjd.21649