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Psoriasis: HELP
Articles by Jonathan Massey
Based on 4 articles published since 2008
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Between 2008 and 2019, J. Massey wrote the following 4 articles about Psoriasis.
 
+ Citations + Abstracts
1 Article Genotypic variability-based genome-wide association study identifies non-additive loci HLA-C and IL12B for psoriasis. 2018

Wei, Wen-Hua / Massey, Jonathan / Worthington, Jane / Barton, Anne / Warren, Richard B. ·Arthritis Research UK Centre for Genetics and Genomics, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK. wenhua.wei@otago.ac.nz. · Department of Women's and Children's Health, Dunedin School of Medicine, University of Otago, Dunedin, 9016, New Zealand. wenhua.wei@otago.ac.nz. · Arthritis Research UK Centre for Genetics and Genomics, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Oxford Road, Manchester, M13 9PT, UK. · NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, M13 9PT, UK. · Dermatology Centre, Salford Royal NHS Foundation Trust, Manchester Academic Health Science Centre, University of Manchester, Manchester, M6 8HD, UK. ·J Hum Genet · Pubmed #29259305.

ABSTRACT: Genome-wide association studies (GWASs) have identified a number of loci for psoriasis but largely ignored non-additive effects. We report a genotypic variability-based GWAS (vGWAS) that can prioritize non-additive loci without requiring prior knowledge of interaction types or interacting factors in two steps, using a mixed model to partition dichotomous phenotypes into an additive component and non-additive environmental residuals on the liability scale and then the Levene's (Brown-Forsythe) test to assess equality of the residual variances across genotype groups genome widely. The vGWAS identified two genome-wide significant (P < 5.0e-08) non-additive loci HLA-C and IL12B that were also genome-wide significant in an accompanying GWAS in the discovery cohort. Both loci were statistically replicated in vGWAS of an independent cohort with a small sample size. HLA-C and IL12B were reported in moderate gene-gene and/or gene-environment interactions in several occasions. We found a moderate interaction with age-of-onset of psoriasis, which was replicated indirectly. The vGWAS also revealed five suggestive loci (P < 6.76e-05) including FUT2 that was associated with psoriasis with environmental aspects triggered by virus infection and/or metabolic factors. Replication and functional investigation are needed to validate the suggestive vGWAS loci.

2 Article Capture Hi-C identifies a novel causal gene, IL20RA, in the pan-autoimmune genetic susceptibility region 6q23. 2016

McGovern, Amanda / Schoenfelder, Stefan / Martin, Paul / Massey, Jonathan / Duffus, Kate / Plant, Darren / Yarwood, Annie / Pratt, Arthur G / Anderson, Amy E / Isaacs, John D / Diboll, Julie / Thalayasingam, Nishanthi / Ospelt, Caroline / Barton, Anne / Worthington, Jane / Fraser, Peter / Eyre, Stephen / Orozco, Gisela. ·Arthritis Research UK Centre for Genetics and Genomics, Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester, Stopford Building, Oxford Road, Manchester, M13 9PT, UK. · Nuclear Dynamics Programme, The Babraham Institute, Cambridge, CB22 3AT, UK. · NIHR Manchester Musculoskeletal BRU, Manchester Academic Health Sciences Centre, Central Manchester Foundation Trust, Manchester, UK. · Institute of Cellular Medicine (Musculoskeletal Research Group), Newcastle University, Newcastle upon Tyne, NE2 4HH, UK. · Center of Experimental Rheumatology Department of Rheumatology, University Hospital of Zurich, Wagistrasse 14, 8952, Schlieren, Switzerland. · Arthritis Research UK Centre for Genetics and Genomics, Division of Musculoskeletal and Dermatological Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester, Stopford Building, Oxford Road, Manchester, M13 9PT, UK. gisela.orozco@manchester.ac.uk. ·Genome Biol · Pubmed #27799070.

ABSTRACT: BACKGROUND: The identification of causal genes from genome-wide association studies (GWAS) is the next important step for the translation of genetic findings into biologically meaningful mechanisms of disease and potential therapeutic targets. Using novel chromatin interaction detection techniques and allele specific assays in T and B cell lines, we provide compelling evidence that redefines causal genes at the 6q23 locus, one of the most important loci that confers autoimmunity risk. RESULTS: Although the function of disease-associated non-coding single nucleotide polymorphisms (SNPs) at 6q23 is unknown, the association is generally assigned to TNFAIP3, the closest gene. However, the DNA fragment containing the associated SNPs interacts through chromatin looping not only with TNFAIP3, but also with IL20RA, located 680 kb upstream. The risk allele of the most likely causal SNP, rs6927172, is correlated with both a higher frequency of interactions and increased expression of IL20RA, along with a stronger binding of both the NFκB transcription factor and chromatin marks characteristic of active enhancers in T-cells. CONCLUSIONS: Our results highlight the importance of gene assignment for translating GWAS findings into biologically meaningful mechanisms of disease and potential therapeutic targets; indeed, monoclonal antibody therapy targeting IL-20 is effective in the treatment of rheumatoid arthritis and psoriasis, both with strong GWAS associations to this region.

3 Article Association of Toll-like receptor 4 (TLR4) with chronic plaque type psoriasis and psoriatic arthritis. 2016

Smith, Rh Ll / Hébert, H L / Massey, J / Bowes, J / Marzo-Ortega, H / Ho, P / McHugh, N J / Worthington, J / Barton, A / Griffiths, C E M / Warren, R B. ·The Dermatology Centre, Salford Royal NHS Foundation Trust, University of Manchester, Manchester Academic Health Science Centre, Manchester, M6 8HD, UK. · Arthritis Research UK Centre for Genetics and Genomics, Centre for Musculoskeletal Research, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK. · NIHR-Leeds Musculoskeletal Biomedical Research Unit, Leeds Institute of Molecular Medicine, University of Leeds, Leeds, UK. · The Kellgren Centre for Rheumatology, Central Manchester Foundation Trust, Manchester, UK. · Royal National Hospital for Rheumatic Diseases and Department of Pharmacy and Pharmacology, University of Bath, Bath, UK. · NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK. · The Dermatology Centre, Salford Royal NHS Foundation Trust, University of Manchester, Manchester Academic Health Science Centre, Manchester, M6 8HD, UK. richard.warren@manchester.ac.uk. ·Arch Dermatol Res · Pubmed #26830904.

ABSTRACT: Family studies have provided overwhelming evidence for an underlying genetic component to psoriasis. Toll-like receptors (TLRs) are key transmembrane proteins in both the innate and adaptive immune responses which are known to be integral processes in psoriasis. Recent functional studies support this notion having suggested a role for TLR4 in the pathogenesis of psoriasis. Furthermore a missense polymorphism in the TLR4 gene has been associated with a number of autoimmune conditions, including Crohn diseases, making TLR4 a viable candidate gene for investigation. The aim of this study was to investigate polymorphisms across the TLR4 region with a high-density single nucleotide polymorphism (SNP) panel in a large cohort of patients with chronic plaque type psoriasis. Twenty SNPs were successfully genotyped using Sequenom iPLEX Gold platform in 2826 UK chronic plaque type psoriasis patients including subgroup data on presence of confirmed psoriatic arthritis (n = 1839) and early-onset psoriasis (n = 1466) was available. Allele frequencies for psoriasis patients were compared against imputed Wellcome Trust Case Control Consortium controls (n = 4861). Significant association was observed between a missense variant rs4986790 of TLR4 (Asp229Gly) and plaque type psoriasis (p = 2 × 10(-4)) which was also notable in those with psoriatic arthritis (p = 2 × 10(-4)) and early-onset psoriasis (p = 8 × 10(-4)). We present data suggestive of an association between a functional variant and an intronic variant of TLR4 and chronic plaque type psoriasis and psoriatic arthritis. However, validation of this association in independent cohorts will be necessary.

4 Article Dense genotyping of immune-related susceptibility loci reveals new insights into the genetics of psoriatic arthritis. 2015

Bowes, John / Budu-Aggrey, Ashley / Huffmeier, Ulrike / Uebe, Steffen / Steel, Kathryn / Hebert, Harry L / Wallace, Chris / Massey, Jonathan / Bruce, Ian N / Bluett, James / Feletar, Marie / Morgan, Ann W / Marzo-Ortega, Helena / Donohoe, Gary / Morris, Derek W / Helliwell, Philip / Ryan, Anthony W / Kane, David / Warren, Richard B / Korendowych, Eleanor / Alenius, Gerd-Marie / Giardina, Emiliano / Packham, Jonathan / McManus, Ross / FitzGerald, Oliver / McHugh, Neil / Brown, Matthew A / Ho, Pauline / Behrens, Frank / Burkhardt, Harald / Reis, Andre / Barton, Anne. ·Arthritis Research UK Centre for Genetics and Genomics, The University of Manchester, Manchester M13 9PT, UK. · 1] Arthritis Research UK Centre for Genetics and Genomics, The University of Manchester, Manchester M13 9PT, UK [2] NIHR Manchester Musculoskeletal Biomedical Research Unit, Central Manchester Foundation Trust and University of Manchester, Manchester Academy of Health Sciences, Manchester M13 9WU, UK. · Institute of Human Genetics, University of Erlangen-Nuremberg, Erlangen 91054, Germany. · 1] Arthritis Research UK Centre for Genetics and Genomics, The University of Manchester, Manchester M13 9PT, UK [2] The Dermatology Centre, Salford Royal NHS Foundation Trust, University of Manchester, Manchester Academic Health Science Centre, Manchester M6 8HD, UK. · 1] JDRF/Wellcome Trust Diabetes and Inflammation Laboratory, Department of Medical Genetics, NIHR Cambridge Biomedical Research Centre, Cambridge Institute for Medical Research, University of Cambridge, Wellcome Trust/MRC Building, Cambridge Biomedical Campus, Cambridge CB2 0XY, UK [2] Centre for Biostatistics, Institute of Population Health, The University of Manchester, Jean McFarlane Building, Oxford Road, Manchester M13 9PL, UK. · 1] Arthritis Research UK Centre for Genetics and Genomics, The University of Manchester, Manchester M13 9PT, UK [2] The Kellgren Centre for Rheumatology, Central Manchester Foundation Trust, NIHR Manchester Biomedical Research Centre, Manchester M13 9WL, UK. · Monash University, Melbourne, Victoria 3800, Australia. · NIHR-Leeds Musculoskeletal Biomedical Research Unit, Leeds Institute of Molecular Medicine, University of Leeds, Leeds LS7 4SA, UK. · CogGene Group, Discipline of Biochemistry and School of Psychology, National University of Ireland, Galway, Ireland. · Department of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin, Dublin 8, Ireland. · Adelaide and Meath Hospital and Trinity College Dublin, Dublin 24, Ireland. · The Dermatology Centre, Salford Royal NHS Foundation Trust, University of Manchester, Manchester Academic Health Science Centre, Manchester M6 8HD, UK. · Royal National Hospital for Rheumatic Diseases and Department of Pharmacy and Pharmacology, University of Bath, Bath BA1 1RL, UK. · Department of Public Health and Clinical Medicine, Rheumatology, University Hospital, Umeå 901 87, Sweden. · Department of Biopathology, Centre of Excellence for Genomic Risk Assessment in Multifactorial and Complex Diseases, School of Medicine, University of Rome 'Tor Vergata' and Fondazione PTV 'Policlinico Tor Vergata', Rome 18-00173, Italy. · Rheumatology Department, Haywood Hospital, Health Services Research Unit, Institute of Science and Technology in Medicine, Keele University, Keele ST5 5BG, UK. · Department of Rheumatology, St. Vincent's University Hospital, UCD School of Medicine and Medical Sciences and Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin 4, Ireland. · The University of Queensland Diamantina Institute, Translational Research Institute, Princess Alexandra Hospital, Brisbane, Queensland QLD 4102, Australia. · Division of Rheumatology and Fraunhofer IME-Project-Group Translational Medicine and Pharmacology, Goethe University, Frankfurt 60590, Germany. ·Nat Commun · Pubmed #25651891.

ABSTRACT: Psoriatic arthritis (PsA) is a chronic inflammatory arthritis associated with psoriasis and, despite the larger estimated heritability for PsA, the majority of genetic susceptibility loci identified to date are shared with psoriasis. Here, we present results from a case-control association study on 1,962 PsA patients and 8,923 controls using the Immunochip genotyping array. We identify eight loci passing genome-wide significance, secondary independent effects at three loci and a distinct PsA-specific variant at the IL23R locus. We report two novel loci and evidence of a novel PsA-specific association at chromosome 5q31. Imputation of classical HLA alleles, amino acids and SNPs across the MHC region highlights three independent associations to class I genes. Finally, we find an enrichment of associated variants to markers of open chromatin in CD8(+) memory primary T cells. This study identifies key insights into the genetics of PsA that could begin to explain fundamental differences between psoriasis and PsA.