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Article
| Open Access
Immunosuppression causes dynamic changes in expression QTLs in psoriatic skin
Psoriasis is a chronic, systemic inflammatory condition primarily affecting skin. Here, the authors investigate the genetic basis of gene expression in skin biopsies from psoriasis patients and interactions with inflammation to better understand mechanisms of the disease.
- Qian Xiao
- , Joseph Mears
- & Soumya Raychaudhuri
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Article
| Open Access
Tenascin C+ papillary fibroblasts facilitate neuro-immune interaction in a mouse model of psoriasis
Local cues for hyperinnervation in chronic skin diseases are not fully understood. Here, the authors show that a distinct subset of dermal papillary fibroblasts promote neurite outgrowth and facilitate neuron-immune interactions through extracellular matrix remodeling in a mouse model of psoriasis
- Xiaojie Cai
- , Maoying Han
- & Honglin Wang
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Article
| Open Access
CD1a promotes systemic manifestations of skin inflammation
Skin inflammation is often accompanied by systemic disease, yet the pathways that regulate this escalation are little known. Here authors show that transgenic expression of human CD1a in mice leads to the escalation of experimental skin inflammation and systemic inflammatory disease, and the generalized symptoms could be alleviated by blocking antibodies developed against CD1a.
- Clare S. Hardman
- , Yi-Ling Chen
- & Graham S. Ogg
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Article
| Open Access
The RNase MCPIP3 promotes skin inflammation by orchestrating myeloid cytokine response
Zinc finger proteins are involved in the resolution of immune responses and function by degrading mRNA of inflammatory cytokines. Here the authors show MCPIP3 promotes skin inflammation via modification of cytokine profiles in pDCs and macrophages.
- Bo Liu
- , Jiancheng Huang
- & Cliff Y. Yang
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Article
| Open Access
TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis
TWEAK is a TNF family member that binds the NFκB signalling receptor Fn14. Here the authors show that TWEAK is central to skin inflammation in mouse models of atopic dermatitis and psoriasis and causes similar pathology when injected subcutaneously into mice.
- Daniel Sidler
- , Ping Wu
- & Michael Croft
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Article
| Open Access
Monocyte-derived inflammatory Langerhans cells and dermal dendritic cells mediate psoriasis-like inflammation
Imiquimod exacerbates IL-23-induced skin inflammation and models psoriasis in mice. Here the authors show that this pathology is not dependent on resident dendritic cells, but on CCR6-induced immigration of monocyte-derived cells.
- Tej Pratap Singh
- , Howard H. Zhang
- & Joshua M. Farber
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Article
| Open Access
IL-12 protects from psoriasiform skin inflammation
IL-12 and IL-23 share the common p40 subunit yet have distinct immunological functions with IL-12 typically contributing to Th1 responses and IL-23 to Th17 responses. Here the authors show that current p40 based therapies for psoriasis are counterproductive owing to an IFN-γ-independent tissue protective function of IL-12 in skin.
- Paulina Kulig
- , Stephanie Musiol
- & Burkhard Becher
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Article
| Open Access
NFATc1 supports imiquimod-induced skin inflammation by suppressing IL-10 synthesis in B cells
Regulatory B cells are important for preventing skin autoimmunity. Here the authors show that NFATc1 suppresses IL-10 transcription in regulatory B cells, and inhibiting NFATc1 decreases immunopathology in a mouse model of imiquimod-induced skin inflammation.
- Hani Alrefai
- , Khalid Muhammad
- & Edgar Serfling
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Article
| Open Access
Antibiotics in neonatal life increase murine susceptibility to experimental psoriasis
Commensal microbes are necessary for proper development of the immune system. Here Zanvit et al. show that neonatal antibiotics treatment causes long-term changes in the gut and skin microbiomes, and exacerbates immune-mediated skin pathology at adult age in mouse experimental models of psoriasis.
- Peter Zanvit
- , Joanne E. Konkel
- & WanJun Chen
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Adiponectin regulates psoriasiform skin inflammation by suppressing IL-17 production from γδ-T cells
Adiponectin levels are decreased in metabolic syndrome and psoriasis patients. Here the authors show that adiponectin suppresses the pathogenic production of IL-17 of γδ T cells, and adiponectin administration improves psoriasis-like symptoms in a mouse model of the disease.
- Sayaka Shibata
- , Yayoi Tada
- & Shinichi Sato
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Article
| Open Access
NF-κB-induced microRNA-31 promotes epidermal hyperplasia by repressing protein phosphatase 6 in psoriasis
Psoriasis is accompanied by NF-κB activation and hyperplasia. Here the authors show that NF-κB transcriptionally activates miR-31, which downregulates a negative cell cycle regulator protein phosphatase 6, and that this is critical for NF-κB to drive keratinocyte hyperproliferation.
- Sha Yan
- , Zhenyao Xu
- & Honglin Wang
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Aquaporin-3-mediated hydrogen peroxide transport is required for NF-κB signalling in keratinocytes and development of psoriasis
Aquaporin-3 (AQP3) mediates cellular uptake of water and hydrogen peroxide (H2O2). Here, the authors show that TNF-induced H2O2enters keratinocytes via AQP3, eliciting NF-κB activation and the development of psoriasis, and identify AQP3 as a potential therapeutic target for this inflammatory immune-mediated disease.
- Mariko Hara-Chikuma
- , Hiroki Satooka
- & A. S. Verkman
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Enhanced meta-analysis and replication studies identify five new psoriasis susceptibility loci
About 2% of the population are affected by psoriasis, a chronic skin disease with complex genetics. Here Tsoi et al.conduct a meta-analysis of several genome-wide association studies and identify five novel loci, helping to further our understanding of the biology behind this condition.
- Lam C. Tsoi
- , Sarah L. Spain
- & James T. Elder
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Article
| Open Access
Genome-wide meta-analysis identifies multiple novel associations and ethnic heterogeneity of psoriasis susceptibility
Psoriasis is a common inflammatory skin disease with complex genetics and different degrees of prevalence across ethnic populations. Here Yin et al. conduct a large trans-ethnic genome-wide meta-analysis and identify novel loci that contribute to population-specific susceptibility.
- Xianyong Yin
- , Hui Qi Low
- & Jianjun Liu
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Article
| Open Access
Whole-exome SNP array identifies 15 new susceptibility loci for psoriasis
Psoriasis is a chronic inflammatory disease affecting up to 3% of the population. Here, Zuo et al.perform exome array analysis, identify single-nucleotide polymorphisms at 15 new loci, implicating several biological pathways in psoriasis risk and disease heritability.
- Xianbo Zuo
- , Liangdan Sun
- & Xuejun Zhang
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The antimicrobial peptide LL37 is a T-cell autoantigen in psoriasis
LL37 is an antimicrobial peptide that is overexpressed in skin lesions from psoriasis patients and activates innate immunity. Here the authors show that CD4 and CD8 T cells specific for LL37 are present in the circulation of patients with psoriasis, produce inflammatory cytokines and correlate with disease activity.
- Roberto Lande
- , Elisabetta Botti
- & Loredana Frasca
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Sequencing-based approach identified three new susceptibility loci for psoriasis
Although psoriasis is a chronic disorder affecting approximately 2% of the population, little is known about the underlying genetic architecture. Here, the authors carry out exome sequencing in a large Han Chinese cohort of psoriasis patients and healthy controls, and identify three new genes that may increase risk of developing the disease.
- Yujun Sheng
- , Xin Jin
- & Xuejun Zhang
Single-atom catalysts-based catalytic ROS clearance for efficient psoriasis treatment and relapse prevention via restoring ESR1