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Psoriasis is a chronic, immune-mediated disorder with cutaneous and systemic manifestations and substantial negative effects on patient quality of life. Psoriasis has a strong, albeit polygenic, genetic basis. Whereas approximately half of the accountable genetic effect of psoriasis maps to the major histocompatibility complex, >70 other loci have been identified, many of which implicate nuclear factor-κB, interferon signalling and the IL-23–IL-23 receptor axis. Psoriasis pathophysiology is characterized by abnormal keratinocyte proliferation and immune cell infiltration in the dermis and epidermis involving the innate and adaptive immune systems, with important roles for dendritic cells and T cells, among other cells. Frequent comorbidities are rheumatological and cardiovascular in nature, in particular, psoriatic arthritis. Current treatments for psoriasis include topical agents, photo-based therapies, traditional systemic drugs and biologic agents. Treatments can be used in combination or as monotherapy. Biologic therapies that target specific disease mediators have become a mainstay in the treatment of moderate-to-severe disease, whereas advances in the treatment of mild-to-moderate disease have been limited.

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Figure 1: Skin manifestations of psoriasis.
Figure 2: Global prevalence of psoriasis.
Figure 3: Evidence of systemic inflammation in patients with psoriasis.
Figure 4: Mechanisms of psoriasis.
Figure 5: Skin biopsy obtained from a patient with psoriasis vulgaris.
Figure 6: Clinical markers of psoriasis.


  1. 1

    Lebwohl, M. Psoriasis. Lancet 361, 1197–1204 (2003). This is a concise, yet comprehensive summary of the understanding of psoriasis pathophysiology and of the topical, light-based and biologic therapies that are used to treat the disease.

  2. 2

    Gudjonsson, J. E. & Elder, J. T. in Fitzpatrick's Dermatology in General Medicine 8th edn (eds Goldmith, L. A. et al.) 197–231 (McGraw-Hill Education, 2012). This is a widely cited textbook chapter on psoriasis.

  3. 3

    Gelfand, J. M. et al. Determinants of quality of life in patients with psoriasis: a study from the US population. J. Am. Acad. Dermatol. 51, 704–708 (2004).

  4. 4

    Kim, N., Thrash, B. & Menter, A. Comorbidities in psoriasis patients. Semin. Cutan. Med. Surg. 29, 10–15 (2010).

  5. 5

    Parisi, R. et al. Global epidemiology of psoriasis: a systematic review of incidence and prevalence. J. Invest. Dermatol. 133, 377–385 (2013). This systematic review summarizes the global incidence and prevalence of psoriasis.

  6. 6

    Tollefson, M. M., Crowson, C. S., McEvoy, M. T. & Maradit Kremers, H. Incidence of psoriasis in children: a population-based study. J. Am. Acad. Dermatol. 62, 979–987 (2010).

  7. 7

    Icen, M. et al. Trends in incidence of adult-onset psoriasis over three decades: a population-based study. J. Am. Acad. Dermatol. 60, 394–401 (2009).

  8. 8

    National Psoriasis Foundation. About psoriasis. National Psoriasis Foundation (accessed 11 Oct 2016).

  9. 9

    Langley, R. G. & Ellis, C. N. Evaluating psoriasis with Psoriasis Area and Severity Index, Psoriasis Global Assessment, and Lattice System Physician's Global Assessment. J. Am. Acad. Dermatol. 51, 563–569 (2004).

  10. 10

    Zachariae, H. et al. Quality of life and prevalence of arthritis reported by 5,795 members of the Nordic Psoriasis Associations. Data from the Nordic Quality of Life Study. Acta Derm. Venereol. 82, 108–113 (2002).

  11. 11

    Gelfand, J. M. et al. Epidemiology of psoriatic arthritis in the population of the United States. J. Am. Acad. Dermatol. 53, 573 (2005).

  12. 12

    Reich, K., Krüger, K., Mössner, R. & Augustin, M. Epidemiology and clinical pattern of psoriatic arthritis in Germany: a prospective interdisciplinary epidemiological study of 1511 patients with plaque-type psoriasis. Br. J. Dermatol. 160, 1040–1047 (2009). This observational, prospective, cohort study demonstrates the substantial number of patients with psoriasis who were treated by dermatologists and had undiagnosed PsA, emphasizing the essential role of dermatologists in evaluating patients with psoriasis for joint involvement.

  13. 13

    Mease, P. J. et al. Prevalence of rheumatologist-diagnosed psoriatic arthritis in patients with psoriasis in European/North American dermatology clinics. J. Am. Acad. Dermatol. 69, 729–735 (2013).

  14. 14

    Gladman, D. D., Antoni, C., Mease, P., Clegg, D. O. & Nash, P. Psoriatic arthritis: epidemiology, clinical features, course, and outcome. Ann. Rheum. Dis. 64 (Suppl. 2), ii14–ii17 (2005). This comprehensive review characterizes the clinical features of PsA and the scope of disease prevalence, which may be underestimated.

  15. 15

    Ahlehoff, O. et al. Cardiovascular disease event rates in patients with severe psoriasis treated with systemic anti-inflammatory drugs: a Danish real-world cohort study. J. Intern. Med. 273, 197–204 (2013).

  16. 16

    Yeung, H. et al. Psoriasis severity and the prevalence of major medical comorbidity: a population-based study. JAMA Dermatol. 149, 1173–1179 (2013).

  17. 17

    Ahlehoff, O. et al. Psoriasis is associated with clinically significant cardiovascular risk: a Danish nationwide cohort study. J. Intern. Med. 270, 147–157 (2011).

  18. 18

    Gelfand, J. M. et al. Risk of myocardial infarction in patients with psoriasis. JAMA 296, 1735–1741 (2006). This population-based, prospective, cohort study from the United Kingdom describes a dose-dependent, increased risk of myocardial infarction among patients with psoriasis.

  19. 19

    Dowlatshahi, E. A. et al. Psoriasis is not associated with atherosclerosis and incident cardiovascular events: the Rotterdam Study. J. Invest. Dermatol. 133, 2347–2354 (2013).

  20. 20

    Wakkee, M., Herings, R. M. & Nijsten, T. Psoriasis may not be an independent risk factor for acute ischemic heart disease hospitalizations: results of a large population-based Dutch cohort. J. Invest. Dermatol. 130, 962–967 (2010).

  21. 21

    Dalgard, F. J. et al. The psychological burden of skin diseases: a cross-sectional multicenter study among dermatological out-patients in 13 European countries. J. Invest. Dermatol. 135, 984–991 (2015).

  22. 22

    Rahman, P. & Elder, J. T. Genetic epidemiology of psoriasis and psoriatic arthritis. Ann. Rheum. Dis. 64 (Suppl. 2), ii37–ii39; discussion ii40–ii41 (2005). This review describes our current understanding of the genetic contributions to psoriasis and PsA and the techniques used in determining these contributions.

  23. 23

    Lonnberg, A. S. et al. Heritability of psoriasis in a large twin sample. Br. J. Dermatol. 169, 412–416 (2013).

  24. 24

    Lonnberg, A. S. et al. Genetic factors explain variation in the age at onset of psoriasis: a population-based twin study. Acta Derm. Venereol. 96, 35–38 (2016).

  25. 25

    Grjibovski, A. M., Olsen, A. O., Magnus, P. & Harris, J. R. Psoriasis in Norwegian twins: contribution of genetic and environmental effects. J. Eur. Acad. Dermatol. Venereol. 21, 1337–1343 (2007).

  26. 26

    Moll, J. M., Wright, V., O'Neill, T. & Silman, A. J. Familial occurrence of psoriatic arthritis. Ann. Rheum. Dis. 32, 181–201 (1973).

  27. 27

    Myers, A., Kay, L. J., Lynch, S. A. & Walker, D. J. Recurrence risk for psoriasis and psoriatic arthritis within sibships. Rheumatology (Oxford) 44, 773–776 (2005).

  28. 28

    Chandran, V. et al. Familial aggregation of psoriatic arthritis. Ann. Rheum. Dis. 68, 664–667 (2009).

  29. 29

    Karason, A., Love, T. J. & Gudbjornsson, B. A strong heritability of psoriatic arthritis over four generations — the Reykjavik Psoriatic Arthritis Study. Rheumatology (Oxford) 48, 1424–1428 (2009).

  30. 30

    Gudjonsson, J. E. & Elder, J. T. Psoriasis: epidemiology. Clin. Dermatol. 25, 535–546 (2007).

  31. 31

    Mahil, S. K., Capon, F. & Barker, J. N. Genetics of psoriasis. Dermatol. Clin. 33, 1–11 (2015).

  32. 32

    Tsoi, L. C. et al. Large-scale meta-analysis identifies 18 novel psoriasis susceptibility loci. Nat. Commun. (in the press).

  33. 33

    Veal, C. D. et al. Family-based analysis using a dense single-nucleotide polymorphism-based map defines genetic variation at PSORS1, the major psoriasis-susceptibility locus. Am. J. Hum. Genet. 71, 554–564 (2002).

  34. 34

    Nair, R. P. et al. Sequence and haplotype analysis supports HLA-C as the psoriasis susceptibility 1 gene. Am. J. Hum. Genet. 78, 827–851 (2006).

  35. 35

    Okada, Y. et al. Fine mapping major histocompatibility complex associations in psoriasis and its clinical subtypes. Am. J. Hum. Genet. 95, 162–172 (2014).

  36. 36

    Fan, X. et al. Fine mapping of the psoriasis susceptibility locus PSORS1 supports HLA-C as the susceptibility gene in the Han Chinese population. PLoS Genet. 4, e1000038 (2008).

  37. 37

    Henseler, T. & Christophers, E. Psoriasis of early and late onset: characterization of two types of psoriasis vulgaris. J. Am. Acad. Dermatol. 13, 450–456 (1985).

  38. 38

    Thorleifsdottir, R. H. et al. HLA-Cw6 homozygosity in plaque psoriasis is associated with streptococcal throat infections and pronounced improvement after tonsillectomy: a prospective case series. J. Am. Acad. Dermatol. 75, 889–896 (2016).

  39. 39

    Sagoo, G. S. et al. Meta-analysis of genome-wide studies of psoriasis susceptibility reveals linkage to chromosomes 6p21 and 4q28–q31 in Caucasian and Chinese Hans population. J. Invest. Dermatol. 122, 1401–1405 (2004).

  40. 40

    Sagoo, G. S., Cork, M. J., Patel, R. & Tazi-Ahnini, R. Genome-wide studies of psoriasis susceptibility loci: a review. J. Dermatol. Sci. 35, 171–179 (2004).

  41. 41

    Karason, A. et al. Genetics of psoriasis in Iceland: evidence for linkage of subphenotypes to distinct loci. J. Invest. Dermatol. 124, 1177–1185 (2005).

  42. 42

    Tomfohrde, J. et al. Gene for familial psoriasis susceptibility mapped to the distal end of human chromosome 17q. Science 264, 1141–1145 (1994).

  43. 43

    Capon, F., Semprini, S., Dallapiccola, B. & Novelli, G. Evidence for interaction between psoriasis-susceptibility loci on chromosomes 6p21 and 1q21 [letter]. Am. J. Hum. Genet. 65, 1798–1800 (1999).

  44. 44

    Veal, C. D. et al. Identification of a novel psoriasis susceptibility locus at 1p and evidence of epistasis between PSORS1 and candidate loci. J. Med. Genet. 38, 7–13 (2001).

  45. 45

    Lee, Y. A. et al. Genomewide scan in german families reveals evidence for a novel psoriasis-susceptibility locus on chromosome 19p13. Am. J. Hum. Genet. 67, 1020–1024 (2000).

  46. 46

    Risch, N. & Merikangas, K. The future of genetic studies of complex human diseases. Science 273, 1516–1517 (1996).

  47. 47

    Yin, X. et al. Genome-wide meta-analysis identifies multiple novel associations and ethnic heterogeneity of psoriasis susceptibility. Nat. Commun. 6, 6916 (2015).

  48. 48

    Zuo, X. et al. Whole-exome SNP array identifies 15 new susceptibility loci for psoriasis. Nat. Commun. 6, 6793 (2015).

  49. 49

    Tsoi, L. C. et al. Enhanced meta-analysis and replication studies identify five new psoriasis susceptibility loci. Nat. Commun. 6, 7001 (2015).

  50. 50

    Tsoi, L. C. et al. Identification of 15 new psoriasis susceptibility loci highlights the role of innate immunity. Nat. Genet. 44, 1341–1348 (2012).

  51. 51

    Bowes, J. et al. Dense genotyping of immune-related susceptibility loci reveals new insights into the genetics of psoriatic arthritis. Nat. Commun. 6, 6046 (2015).

  52. 52

    Stuart, P. E. et al. Genome-wide association analysis of psoriatic arthritis and cutaneous psoriasis reveals differences in their genetic architecture. Am. J. Hum. Genet. 97, 816–836 (2015).

  53. 53

    Bowes, J. et al. PTPN22 is associated with susceptibility to psoriatic arthritis but not psoriasis: evidence for a further PsA-specific risk locus. Ann. Rheum. Dis. 74, 1882–1885 (2015).

  54. 54

    Shendure, J. & Lieberman Aiden, E. The expanding scope of DNA sequencing. Nat. Biotechnol. 30, 1084–1094 (2012).

  55. 55

    Mossner, R. et al. Palmoplantar pustular psoriasis is associated with missense variants in CARD14, but not with loss-of-function mutations in IL36RN in European patients. J. Invest. Dermatol. 135, 2538–2541 (2015).

  56. 56

    Jordan, C. T. et al. PSORS2 is due to mutations in CARD14. Am. J. Hum. Genet. 90, 784–795 (2012).

  57. 57

    Setta-Kaffetzi, N. et al. AP1S3 mutations are associated with pustular psoriasis and impaired Toll-like receptor 3 trafficking. Am. J. Hum. Genet. 94, 790–797 (2014).

  58. 58

    Marrakchi, S. et al. Interleukin-36-receptor antagonist deficiency and generalized pustular psoriasis. N. Engl. J. Med. 365, 620–628 (2011).

  59. 59

    Onoufriadis, A. et al. Mutations in IL36RN/IL1F5 are associated with the severe episodic inflammatory skin disease known as generalized pustular psoriasis. Am. J. Hum. Genet. 89, 432–437 (2011).

  60. 60

    Setta-Kaffetzi, N. et al. Rare pathogenic variants in IL36RN underlie a spectrum of psoriasis-associated pustular phenotypes. J. Invest. Dermatol. 133, 1366–1369 (2013).

  61. 61

    Capon, F. IL36RN mutations in generalized pustular psoriasis: just the tip of the iceberg?. J. Invest. Dermatol. 133, 2503–2504 (2013).

  62. 62

    Edwards, S. L., Beesley, J., French, J. D. & Dunning, A. M. Beyond GWASs: illuminating the dark road from association to function. Am. J. Hum. Genet. 93, 779–797 (2013).

  63. 63

    Tsoi, L. C., Elder, J. T. & Abecasis, G. R. Graphical algorithm for integration of genetic and biological data: proof of principle using psoriasis as a model. Bioinformatics 31, 1243–1249 (2015).

  64. 64

    Swindell, W. R. et al. Psoriasis drug development and GWAS interpretation through in silico analysis of transcription factor binding sites. Clin. Transl Med. 4, 13 (2015).

  65. 65

    Suzuki, E., Mellins, E. D., Gershwin, M. E., Nestle, F. O. & Adamopoulos, I. E. The IL-23/IL-17 axis in psoriatic arthritis. Autoimmun. Rev. 13, 496–502 (2014).

  66. 66

    Lande, R. et al. Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide. Nature 449, 564–569 (2007).

  67. 67

    Zheng, Y. et al. Interleukin-22, a TH17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis. Nature 445, 648–651 (2007).

  68. 68

    Man, X. Y., Yang, X. H., Cai, S. Q., Bu, Z. Y. & Zheng, M. Overexpression of vascular endothelial growth factor (VEGF) receptors on keratinocytes in psoriasis: regulated by calcium independent of VEGF. J. Cell. Mol. Med. 12, 649–660 (2008).

  69. 69

    Tauber, M. et al. IL36RN mutations affect protein expression and function: a basis for genotype–phenotype correlation in pustular diseases. J. Invest. Dermatol. 136, 1811–1819 (2016).

  70. 70

    Lizzul, P. F. et al. Differential expression of phosphorylated NF-κB/RelA in normal and psoriatic epidermis and downregulation of NF-κB in response to treatment with etanercept. J. Invest. Dermatol. 124, 1275–1283 (2005).

  71. 71

    Raphael, I., Nalawade, S., Eagar, T. N. & Forsthuber, T. G. T cell subsets and their signature cytokines in autoimmune and inflammatory diseases. Cytokine 74, 5–17 (2015). This is an overview of the role of TH cell subsets and associated cytokine profiles in the development of inflammatory diseases, including psoriasis, in which T cell activity has a central function.

  72. 72

    Zhu, J. & Paul, W. E. Heterogeneity and plasticity of T helper cells. Cell Res. 20, 4–12 (2010).

  73. 73

    Chiricozzi, A. et al. IL-17 induces an expanded range of downstream genes in reconstituted human epidermis model. PLoS ONE 9, e90284 (2014).

  74. 74

    Nestle, F. O. et al. Plasmacytoid predendritic cells initiate psoriasis through interferon-α production. J. Exp. Med. 202, 135–143 (2005).

  75. 75

    Gladman, D. D. Clinical features and diagnostic considerations in psoriatic arthritis. Rheum. Dis. Clin. North Am. 41, 569–579 (2015).

  76. 76

    Feldman, S. R. & Krueger, G. G. Psoriasis assessment tools in clinical trials. Ann. Rheum. Dis. 64 (Suppl. 2), ii65–ii68; discussion ii69–ii73 (2005).

  77. 77

    Samman, P. D. & Fenton, D. A. Samman's The Nails in Disease 5th edn (Butterworth-Heinemann, 1995).

  78. 78

    Menter, A. et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. J. Am. Acad. Dermatol. 58, 826–850 (2008).

  79. 79

    Gladman, D. D. & Rosen, C. T. Psoriatic Arthritis (The Facts) (Oxford Univ. Press, 2008).

  80. 80

    Haroon, M., Kirby, B. & FitzGerald, O. High prevalence of psoriatic arthritis in patients with severe psoriasis with suboptimal performance of screening questionnaires. Ann. Rheum. Dis. 72, 736–740 (2013).

  81. 81

    Eder, L., Chandran, V. & Gladman, D. D. What have we learned about genetic susceptibility in psoriasis and psoriatic arthritis? Curr. Opin. Rheumatol 27, 91–98 (2015).

  82. 82

    Chandran, V. et al. Soluble biomarkers differentiate patients with psoriatic arthritis from those with psoriasis without arthritis. Rheumatology (Oxford) 49, 1399–1405 (2010).

  83. 83

    Ritchlin, C. T. et al. Treatment recommendations for psoriatic arthritis. Ann. Rheum. Dis. 68, 1387–1394 (2009).

  84. 84

    Taylor, W. et al. Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arthritis Rheum. 54, 2665–2673 (2006).

  85. 85

    Haroon, M., Gallagher, P. & FitzGerald, O. Diagnostic delay of more than 6 months contributes to poor radiographic and functional outcome in psoriatic arthritis. Ann. Rheum. Dis. 74, 1045–1050 (2015).

  86. 86

    Wilson, P. W. et al. Prediction of coronary heart disease using risk factor categories. Circulation 97, 1837–1847 (1998).

  87. 87

    Mehta, N. N. et al. Attributable risk estimate of severe psoriasis on major cardiovascular events. Am. J. Med. 124, 775.e1–775.e6 (2011). This retrospective, cohort study demonstrates the absolute risk of major adverse cardiovascular events in patients with psoriasis, particularly those with severe cutaneous involvement, compared with the general population.

  88. 88

    Goff, D. C. et al. 2013 ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 129, S49–S73 (2014).

  89. 89

    European Association for Cardiovascular Prevention & Rehabilitation et al. ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS). Eur. Heart J. 32, 1769–1818 (2011).

  90. 90

    Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA 285, 2486–2497 (2001).

  91. 91

    Jokai, H. et al. Impact of effective tumor necrosis factor-alfa inhibitor treatment on arterial intima-media thickness in psoriasis: results of a pilot study. J. Am. Acad. Dermatol. 69, 523–529 (2013).

  92. 92

    Bissonnette, R. et al. Effects of the tumor necrosis factor-alpha antagonist adalimumab on arterial inflammation assessed by positron emission tomography in patients with psoriasis: results of a randomized controlled trial. Circ. Cardiovasc. Imaging 6, 83–90 (2013).

  93. 93

    Wu, J. J., Poon, K. Y., Channual, J. C. & Shen, A. Y. Association between tumor necrosis factor inhibitor therapy and myocardial infarction risk in patients with psoriasis. Arch. Dermatol. 148, 1244–1250 (2012). This cohort study demonstrates a decreased risk of myocardial infarction among patients with psoriasis who were treated with TNF inhibitors, with key implications about the potential systemic effect of psoriasis and the broader role of treatments on patient health.

  94. 94

    US National Library of Medicine. ClinicalTrials.gov (2016).

  95. 95

    US National Library of Medicine. ClinicalTrials.gov (2016).

  96. 96

    American Academy of Dermatology Work Group et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 6. Guidelines of care for the treatment of psoriasis and psoriatic arthritis: case-based presentations and evidence-based conclusions. J. Am. Acad. Dermatol. 65, 137–174 (2011). This is the most recent set of treatment guidelines produced by leaders in the field of psoriasis, with a set of case-based examples to illustrate evidence-based recommendations.

  97. 97

    Nast, A. et al. European S3-guidelines on the systemic treatment of psoriasis vulgaris — update 2015 — short version — EDF in cooperation with EADV and IPC. J. Eur.Acad. Dermatol. Venereol. 29, 2277–2294 (2015). This is a set of guidelines from an international group of dermatologists with graded recommendations for systemic treatments of psoriasis.

  98. 98

    McGill, A. et al. The anti-psoriatic drug anthralin accumulates in keratinocyte mitochondria, dissipates mitochondrial membrane potential, and induces apoptosis through a pathway dependent on respiratory competent mitochondria. FASEB J. 19, 1012–1014 (2005).

  99. 99

    Arbiser, J. L. et al. Carbazole is a naturally occurring inhibitor of angiogenesis and inflammation isolated from antipsoriatic coal tar. J. Invest. Dermatol. 126, 1396–1402 (2006).

  100. 100

    Rizova, E. & Corroller, M. Topical calcitriol — studies on local tolerance and systemic safety. Br. J. Dermatol. 144 (Suppl. 58), 3–10 (2001).

  101. 101

    Lebwohl, M. G. et al. Tazarotene 0. 1% gel plus corticosteroid cream in the treatment of plaque psoriasis. J. Am. Acad. Dermatol. 39, 590–596 (1998).

  102. 102

    Freeman, A. K. et al. Tacrolimus ointment for the treatment of psoriasis on the face and intertriginous areas. J. Am. Acad. Dermatol. 48, 564–568 (2003).

  103. 103

    Tartar, D., Bhutani, T., Huynh, M., Berger, T. & Koo, J. Update on the immunological mechanism of action behind phototherapy. J. Drugs Dermatol. 13, 564–568 (2014).

  104. 104

    Goeckerman, W. H. Treatment of psoriasis. Northwest Med. 24, 229–231 (1925).

  105. 105

    Pittelkow, M. R. et al. Skin cancer in patients with psoriasis treated with coal tar. A 25-year follow-up study. Arch. Dermatol. 117, 465–468 (1981).

  106. 106

    Nolan, B. V., Yentzer, B. A. & Feldman, S. R. A review of home phototherapy for psoriasis. Dermatol. Online J. 16, 1 (2010).

  107. 107

    Stern, R. S. & PUVA Follow-Up Study. The risk of squamous cell and basal cell cancer associated with psoralen and ultraviolet A therapy: a 30-year prospective study. J. Am. Acad. Dermatol. 66, 553–562 (2012).

  108. 108

    Stern, R. S. & PUVA Follow-Up Study. The risk of melanoma in association with long-term exposure to PUVA. J. Am. Acad. Dermatol. 44, 755–761 (2001).

  109. 109

    Menter, A. et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 4. Guidelines of care for the management and treatment of psoriasis with traditional systemic agents. J. Am. Acad. Dermatol. 61, 451–485 (2009).

  110. 110

    Cronstein, B. N., Naime, D. & Ostad, E. The antiinflammatory mechanism of methotrexate. Increased adenosine release at inflamed sites diminishes leukocyte accumulation in an in vivo model of inflammation. J. Clin. Invest. 92, 2675–2682 (1993).

  111. 111

    Majumdar, S. & Aggarwal, B. B. Methotrexate suppresses NF-κB activation through inhibition of IκBα phosphorylation and degradation. J. Immunol. 167, 2911–2920 (2001).

  112. 112

    Goldminz, A. M. et al. Methotrexate improves pro- and anti-atherogenic genomic expression in psoriatic skin. J. Dermatol. Sci. 82, 207–209 (2016).

  113. 113

    Gutierrez-Urena, S., Molina, J. F., Garcia, C. O., Cuellar, M. L. & Espinoza, L. R. Pancytopenia secondary to methotrexate therapy in rheumatoid arthritis. Arthritis Rheum. 39, 272–276 (1996).

  114. 114

    Al-Quteimat, O. M. & Al-Badaineh, M. A. Methotrexate and trimethoprim-sulphamethoxazole: extremely serious and life-threatening combination. J. Clin. Pharm. Ther. 38, 203–205 (2013).

  115. 115

    Rosenberg, P. et al. Psoriasis patients with diabetes type 2 are at high risk of developing liver fibrosis during methotrexate treatment. J. Hepatol. 46, 1111–1118 (2007).

  116. 116

    Kalb, R. E., Strober, B., Weinstein, G. & Lebwohl, M. Methotrexate and psoriasis: consensus conference. J. Am. Acad. Dermatol. 64, 1179 (2011).

  117. 117

    Boffa, M. J. et al. Serum type III procollagen aminopeptide for assessing liver damage in methotrexate-treated psoriatic patients. Br. J. Dermatol. 135, 538–544 (1996).

  118. 118

    Raposo, I. & Torres, T. Palmoplantar psoriasis and palmoplantar pustulosis: current treatment and future prospects. Am. J. Clin. Dermatol. 17, 349–358 (2016).

  119. 119

    Lebwohl, M. et al. Consensus conference: acitretin in combination with UVB or PUVA in the treatment of psoriasis. J. Am. Acad. Dermatol. 45, 544–553 (2001).

  120. 120

    Niu, X. et al. Acitretin exerted a greater influence on T-helper (Th)1 and Th17 than on Th2 cells in treatment of psoriasis vulgaris. J. Dermatol. 39, 916–921 (2012).

  121. 121

    Katz, H. I., Waalen, J. & Leach, E. E. Acitretin in psoriasis: an overview of adverse effects. J. Am. Acad. Dermatol. 41, S7–S12 (1999).

  122. 122

    Amor, K. T., Ryan, C. & Menter, A. The use of cyclosporine in dermatology: part I. J. Am. Acad. Dermatol. 63, 925–946 (2010).

  123. 123

    Zachariae, H., Kragballe, K., Hansen, H. E., Marcussen, N. & Olsen, S. Renal biopsy findings in long-term cyclosporin treatment of psoriasis. Br. J. Dermatol. 136, 531–535 (1997).

  124. 124

    Schafer, P. Apremilast mechanism of action and application to psoriasis and psoriatic arthritis. Biochem. Pharmacol. 83, 1583–1590 (2012).

  125. 125

    Paul, C. et al. Efficacy and safety of apremilast, an oral phosphodiesterase 4 inhibitor, in patients with moderate-to-severe plaque psoriasis over 52 weeks: a phase III, randomized controlled trial (ESTEEM 2). Br. J. Dermatol. 173, 1387–1399 (2015).

  126. 126

    Papp, K. et al. Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor, in patients with moderate to severe plaque psoriasis: results of a phase III, randomized, controlled trial (Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis [ESTEEM] 1). J. Am. Acad. Dermatol. 73, 37–49 (2015).

  127. 127

    Atwan, A. et al. Oral fumaric acid esters for psoriasis: abridged Cochrane systematic review including GRADE assessments. Br. J. Dermatol. 175, 873–881 (2016).

  128. 128

    Ghoreschi, K. et al. Fumarates improve psoriasis and multiple sclerosis by inducing type II dendritic cells. J. Exp. Med. 208, 2291–2303 (2011).

  129. 129

    Zweegers, J. et al. Body mass index predicts discontinuation due to ineffectiveness and female sex predicts discontinuation due to side-effects in patients with psoriasis treated with adalimumab, etanercept or ustekinumab in daily practice: a prospective, comparative, long-term drug-survival study from the BioCAPTURE registry. Br. J. Dermatol. 175, 340–347 (2016).

  130. 130

    Gottlieb, A. et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 2. Psoriatic arthritis: overview and guidelines of care for treatment with an emphasis on the biologics. J. Am. Acad. Dermatol. 58, 851–864 (2008).

  131. 131

    Dixon, W. G. et al. Reduction in the incidence of myocardial infarction in patients with rheumatoid arthritis who respond to anti-tumor necrosis factor alpha therapy: results from the British Society for Rheumatology Biologics Register. Arthritis Rheum. 56, 2905–2912 (2007).

  132. 132

    Hoffman, M. B., Farhangian, M. & Feldman, S. R. Psoriasis during pregnancy: characteristics and important management recommendations. Expert Rev. Clin. Immunol. 11, 709–720 (2015).

  133. 133

    Bongartz, T. et al. Anti-TNF antibody therapy in rheumatoid arthritis and the risk of serious infections and malignancies: systematic review and meta-analysis of rare harmful effects in randomized controlled trials. JAMA 295, 2275–2285 (2006).

  134. 134

    Papp, K. A. et al. Long-term safety of ustekinumab in patients with moderate-to-severe psoriasis: final results from 5 years of follow-up. Br. J. Dermatol. 168, 844–854 (2013)

  135. 135

    Collamer, A. N., Guerrero, K. T., Henning, J. S. & Battafarano, D. F. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: a literature review and potential mechanisms of action. Arthritis Rheum. 59, 996–1001 (2008).

  136. 136

    Doherty, S. D. et al. National Psoriasis Foundation consensus statement on screening for latent tuberculosis infection in patients with psoriasis treated with systemic and biologic agents. J. Am. Acad. Dermatol. 59, 209–217 (2008).

  137. 137

    Kavanaugh, A. et al. Maintenance of clinical efficacy and radiographic benefit through two years of ustekinumab therapy in patients with active psoriatic arthritis: results from a randomized, placebo-controlled phase III trial. Arthritis Care Res. (Hoboken) 67, 1739–1749 (2015).

  138. 138

    McInnes, I. B. et al. Secukinumab, a human anti-interleukin-17A monoclonal antibody, in patients with psoriatic arthritis (FUTURE 2): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet 386, 1137–1146 (2015).

  139. 139

    Elyoussfi, S., Thomas, B. J. & Ciurtin, C. Tailored treatment options for patients with psoriatic arthritis and psoriasis: review of established and new biologic and small molecule therapies. Rheumatol. Int. 36, 603–612 (2016).

  140. 140

    Mease, P. J. et al. Brodalumab, an anti-IL17RA monoclonal antibody, in psoriatic arthritis. N. Engl. J. Med. 370, 2295–2306 (2014).

  141. 141

    Lebwohl, M. et al. Phase 3 studies comparing brodalumab with ustekinumab in psoriasis. N. Engl. J. Med. 373, 1318–1328 (2015).

  142. 142

    Ling, Y. & Puel, A. IL-17 and infections. Actas Dermosifiliogr. 105 (Suppl. 1), 34–40 (2014).

  143. 143

    Papp, K. A. et al. A prospective phase III, randomized, double-blind, placebo-controlled study of brodalumab in patients with moderate-to-severe plaque psoriasis. Br. J. Dermatol. 175, 273–286 (2016).

  144. 144

    Sicotte, N. L. & Voskuhl, R. R. Onset of multiple sclerosis associated with anti-TNF therapy. Neurology 57, 1885–1888 (2001).

  145. 145

    Young, M. S., Horn, E. J. & Cather, J. C. The ACCEPT study: ustekinumab versus etanercept in moderate-to-severe psoriasis patients. Expert Rev. Clin. Immunol. 7, 9–13 (2011).

  146. 146

    Thaci, D. et al. Secukinumab is superior to ustekinumab in clearing skin of subjects with moderate to severe plaque psoriasis: CLEAR, a randomized controlled trial. J. Am. Acad. Dermatol. 73, 400–409 (2015).

  147. 147

    Betts, K. A., Mittal, M., Joshi, A., Song, J. & Bao, Y. Relative efficacy of adalimumab versus secukinumab in active psoriatic arthritis: a matching-adjusted indirect comparison. Arthritis Rheumatol. Abstr. 67 (Suppl. 10), 2868 (2015).

  148. 148

    Hsu, L., Snodgrass, B. T. & Armstrong, A. W. Antidrug antibodies in psoriasis: a systematic review. Br. J. Dermatol. 170, 261–273 (2014).

  149. 149

    Dapavo, P., Vujic, I., Fierro, M. T., Quaglino, P. & Sanlorenzo, M. The infliximab biosimilar in the treatment of moderate to severe plaque psoriasis. J. Am. Acad. Dermatol. 75, 736–739 (2016).

  150. 150

    Red. [First biosimilar etanercept is available]. MMW Fortschritte der Medizin 158, 82 (in German) (2016).

  151. 151

    de Korte, J., Sprangers, M. A., Mombers, F. M. & Bos, J. D. Quality of life in patients with psoriasis: a systematic literature review. J. Invest. Dermatol. Symp. Proc. 9, 140–147 (2004).

  152. 152

    Lee, Y. W., Park, E. J., Kwon, I. H., Kim, K. H. & Kim, K. J. Impact of psoriasis on quality of life: relationship between clinical response to therapy and change in health-related quality of life. Ann. Dermatol. 22, 389–396 (2010). This prospective, cohort study demonstrates the improvement in patients' health-related QOL measures after treatment, and elucidates key factors that make psoriasis more burdensome, emphasizing the important role of health care providers and the profound effect of psoriasis treatments on disease burden.

  153. 153

    Bhatti, Z. U. et al. Chronic disease influences over 40 major life-changing decisions (MLCDs): a qualitative study in dermatology and general medicine. J. Eur. Acad. Dermatol. Venereol. 28, 1344–1355 (2014).

  154. 154

    Eghlileb, A. M., Davies, E. E. & Finlay, A. Y. Psoriasis has a major secondary impact on the lives of family members and partners. Br. J. Dermatol. 156, 1245–1250 (2007).

  155. 155

    Iskandar, I. Y. et al. Demographics and disease characteristics of patients with psoriasis enrolled in the British Association of Dermatologists Biologic Interventions Register. Br. J. Dermatol. 173, 510–518 (2015).

  156. 156

    Basra, M. K., Fenech, R., Gatt, R. M., Salek, M. S. & Finlay, A. Y. The Dermatology Life Quality Index 1994–2007: a comprehensive review of validation data and clinical results. Br. J. Dermatol. 159, 997–1035 (2008).

  157. 157

    Finlay, A. Y. Current severe psoriasis and the rule of tens. Br. J. Dermatol. 152, 861–867 (2005).

  158. 158

    Ali, F. M. et al. A systematic review of the use of quality of life instruments in randomised controlled trials of psoriasis. Br J. Dermatol. (2016).

  159. 159

    Moller, A. H., Erntoft, S., Vinding, G. R. & Jemec, G. B. A systematic literature review to compare quality of life in psoriasis with other chronic diseases using EQ-5D-derived utility values. Patient Relat. Outcome Meas. 6, 167–177 (2015). This systematic review demonstrates that the burden of psoriatic disease is comparable to that of other chronic diseases, including cardiovascular disease and diabetes.

  160. 160

    Takahashi, H., Iinuma, S., Tsuji, H., Honma, M. & Iizuka, H. Biologics are more potent than other treatment modalities for improvement of quality of life in psoriasis patients. J. Dermatol. 41, 686–689 (2014).

  161. 161

    Stein, K. R., Pearce, D. J. & Feldman, S. R. The impact of biologics on the quality of life of psoriasis patients and the economics of psoriasis care. Semin. Cutan. Med. Surg. 24, 52–57 (2005).

  162. 162

    Larsen, M. H., Hagen, K. B., Krogstad, A. L., Aas, E. & Wahl, A. K. Limited evidence of the effects of patient education and self-management interventions in psoriasis patients: a systematic review. Patient Educ. Couns. 94, 158–169 (2014).

  163. 163

    Gedebjerg, A., Johansen, C., Kragballe, K. & Iversen, L. IL-20, IL-21 and p40: potential biomarkers of treatment response for ustekinumab. Acta Derm. Venereol. 93, 150–155 (2013).

  164. 164

    Ryan, C. et al. Research gaps in psoriasis: opportunities for future studies. J. Am. Acad. Dermatol. 70, 146–167 (2014).

  165. 165

    Armstrong, A. W., Gelfand, J. M., Boehncke, W. H. & Armstrong, E. J. Cardiovascular comorbidities of psoriasis and psoriatic arthritis: a report from the GRAPPA 2012 annual meeting. J. Rheumatol. 40, 1434–1437 (2013).

  166. 166

    Kirkham, B. et al. Early treatment of psoriatic arthritis is associated with improved patient-reported outcomes: findings from the etanercept PRESTA trial. Clin. Exp. Rheumatol. 33, 11–19 (2015).

  167. 167

    Kimball, A. B. et al. National Psoriasis Foundation clinical consensus on psoriasis comorbidities and recommendations for screening. J. Am. Acad. Dermatol. 58, 1031–1042 (2008).

  168. 168

    Capon, F. & Barker, J. N. The quest for psoriasis susceptibility genes in the postgenome-wide association studies era: charting the road ahead. Br. J. Dermatol. 166, 1173–1175 (2012).

  169. 169

    Alwan, W. & Nestle, F. O. Pathogenesis and treatment of psoriasis: exploiting pathophysiological pathways for precision medicine. Clin. Exp. Rheumatol 33, S2–S6 (2015). This review elucidates future areas of psoriasis research based on the trend towards highly precise targeted therapies.

  170. 170

    Zweegers, J. et al. Effectiveness of biologic and conventional systemic therapies in adults with chronic plaque psoriasis in daily practice: a systematic review. Acta Derm. Venereol. 96, 453–458 (2016).

  171. 171

    De Mozzi, P., Johnston, G. A., Alexandroff, A. B. Psoriasis: an evidence-based update. Report of the 9th evidenced based update meeting, 12 May 2011, Loughborough, UK. Br. J. Dermatol. 166, 252–260 (2012).

  172. 172

    Eissing, L., Radtke, M. A., Zander, N. & Augustin, M. Barriers to guideline-compliant psoriasis care: analyses and concepts. J. Eur. Acad. Dermatol. Venereol. 30, 569–575 (2016).

  173. 173

    FitzGerald, O. & Mease, P. J. Biomarkers: project update from the GRAPPA 2012 annual meeting. J. Rheumatol. 40, 1453–1454 (2013).

  174. 174

    FitzGerald, O., Mease, P. J., Helliwell, P. S. & Chandran, V. GRAPPA 2013 annual meeting, rheumatology updates: psoriatic arthritis (PsA) biomarker project, arthritis mutilans, PsA-peripheral spondyloarthritis epidemiology project. J. Rheumatol. 41, 1244–1248 (2014).

  175. 175

    Villanova, F., Di Meglio, P. & Nestle, F. O. Biomarkers in psoriasis and psoriatic arthritis. Ann. Rheum. Dis. 72 (Suppl. 2), ii104–ii110 (2013).

  176. 176

    Armstrong, A. W., Robertson, A. D., Wu, J., Schupp, C. & Lebwohl, M. G. Undertreatment, treatment trends, and treatment dissatisfaction among patients with psoriasis and psoriatic arthritis in the United States: findings from the National Psoriasis Foundation surveys, 2003–2011. JAMA Dermatol. 149, 1180–1185 (2013).

  177. 177

    Croughan, M. S., Konstantinov, K. B. & Cooney, C. The future of industrial bioprocessing: batch or continuous? Biotechnol. Bioeng. 112, 648–651 (2015).

  178. 178

    Gottlieb, A. B. et al. The International Dermatology Outcome Measures Group: formation of patient-centered outcome measures in dermatology. J. Am. Acad. Dermatol. 72, 345–348 (2015).

  179. 179

    Tan, K. W. & Griffiths, C. E. Novel systemic therapies for the treatment of psoriasis. Expert Opin. Pharmacother. 17, 79–92 (2016).

  180. 180

    Feely, M. A., Smith, B. L. & Weinberg, J. M. Novel psoriasis therapies and patient outcomes, part 1: topical medications. Cutis 95, 164–168, 170 (2015).

  181. 181

    Rahman, M. et al. Nanomedicine-based drug targeting for psoriasis: potentials and emerging trends in nanoscale pharmacotherapy. Expert Opin. Drug Deliv. 12, 635–652 (2015).

  182. 182

    Yin, X. et al. A weighted polygenic risk score using 14 known susceptibility variants to estimate risk and age onset of psoriasis in Han Chinese. PLoS ONE 10, e0125369 (2015).

  183. 183

    Latchman, D. S. Transcription-factor mutations and disease. N. Engl. J. Med. 334, 28–33 (1996).

  184. 184

    Sano, S. et al. Stat3 links activated keratinocytes and immunocytes required for development of psoriasis in a novel transgenic mouse model. Nat. Med. 11, 43–49 (2005).

  185. 185

    Kryczek, I. et al. Induction of IL-17+ T cell trafficking and development by IFN-γ: mechanism and pathological relevance in psoriasis. J. Immunol. 181, 4733–4741 (2008).

  186. 186

    Harden, J. L. et al. Humanized anti-IFN-γ (HuZAF) in the treatment of psoriasis. J. Allergy Clin. Immunol. 135, 553–556 (2015).

  187. 187

    National Psoriasis Foundation. Drug pipeline 2016. National Psoriasis Foundation (accessed 7 Oct 2016).

  188. 188

    Papp, K. A. et al. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 52-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 2). Lancet 371, 1675–1684 (2008).

  189. 189

    Baldassare, J. J., Fisher, G. J., Henderson, P. A. & Voorhees, J. J. Epidermal growth factor (EGF) stimulates phosphatidylcholine hydrolysis by phospholipases c and d in human dermal fibroblasts (meeting abstract). FASEB J. 4, A2059 (1990).

  190. 190

    Mease, P. J., Garg, A., Helliwell, P. S., Park, J. J. & Gladman, D. D. Development of criteria to distinguish inflammatory from noninflammatory arthritis, enthesitis, dactylitis, and spondylitis: a report from the GRAPPA 2013 annual meeting. J. Rheumatol. 41, 1249–1251 (2014).

  191. 191

    Gladman, D. D., Helliwell, P. S., Khraishi, M., Callis Duffin, K. & Mease, P. J. Dermatology screening tools: project update from the GRAPPA 2012 annual meeting. J. Rheumatol. 40, 1425–1427 (2013).

  192. 192

    Tom, B. D., Chandran, V., Farewell, V. T., Rosen, C. F. & Gladman, D. D. Validation of the Toronto Psoriatic Arthritis Screen Version 2 (ToPAS 2). J. Rheumatol. 42, 841–846 (2015).

  193. 193

    Bronsard, V. et al. What are the best outcome measures for assessing quality of life in plaque type psoriasis? A systematic review of the literature. J. Eur. Acad. Dermatol. Venereol. 24 (Suppl. 2), 17–22 (2010).

  194. 194

    Pedersen, C. B. et al. Reliability and validity of the Psoriasis Itch Visual Analog Scale in psoriasis vulgaris. J. Dermatol. Treat. 5 Sept 2016 [epub ahead of print].

  195. 195

    Bushnell, D. M. et al. Validation of the Psoriasis Symptom Inventory (PSI), a patient-reported outcome measure to assess psoriasis symptom severity. J. Dermatol. Treat. 24, 356–360 (2013).

  196. 196

    Fotiou, K., Hofmann, M., Kaufmann, R. & Thaci, D. Pictorial representation of illness and self measure (PRISM): an effective tool to assess the burden of psoriasis. J. Eur. Acad. Dermatol. Venereol. 29, 2356–2362 (2015).

  197. 197

    Holme, S. A. et al. The Children's Dermatology Life Quality Index: validation of the cartoon version. Br. J. Dermatol. 148, 285–290 (2003).

  198. 198

    Eghlileb, A. M., Basra, M. K. & Finlay, A. Y. The Psoriasis Family Index: preliminary results of validation of a quality of life instrument for family members of patients with psoriasis. Dermatology 219, 63–70 (2009).

  199. 199

    Finlay, A. Y., Salek, S. S. & Piguet, V. Measuring family impact of skin diseases: FDLQI and FROM-16. Acta Derm. Venereol. 95, 1036 (2015).

  200. 200

    Jacobson, C. C., Kumar, S. & Kimball, A. B. Latitude and psoriasis prevalence. J. Am. Acad. Dermatol. 65, 870–873 (2011).

  201. 201

    Williams, H. C. & Strachan, D. P. The Challenge of Dermato-Epidemiology (CRC Press, 1997).

  202. 202

    Grob, J. J. in Textbook of Psoriasis (ed. van de Kerkhof, P. C. M. ) 57–69 (Blackwell Publishing, 2003).

  203. 203

    Yip, S. Y. The prevalence of psoriasis in the Mongoloid race. J. Am. Acad. Dermatol. 10, 965–968 (1984).

  204. 204

    International Psoriasis Council. IPC psoriasis review. IPC (2016).

  205. 205

    Alexis, A. F. & Blackcloud, P. Psoriasis in skin of color: epidemiology, genetics, clinical presentation, and treatment nuances. J. Clin. Aesthet. Dermatol. 7, 16–24 (2014).

  206. 206

    International Psoriasis Council. IPC psoriasis review focus on Latin America. IPC (2009).

  207. 207

    Imafuku, S., Naito, R. & Nakayama, J. Possible association of hepatitis C virus infection with late-onset psoriasis: a hospital-based observational study. J. Dermatol. 40, 813–818 (2013).

  208. 208

    Kim, T. G. et al. Dermal clusters of mature dendritic cells and T cells are associated with the CCL20/CCR6 chemokine system in chronic psoriasis. J. Invest. Dermatol. 134, 1462–1465 (2014).

  209. 209

    Mease, P. J. et al. Continued inhibition of radiographic progression in patients with psoriatic arthritis following 2 years of treatment with etanercept. J. Rheumatol. 33, 712–721 (2006).

  210. 210

    Leonardi, C. L. et al. Etanercept as monotherapy in patients with psoriasis. N. Engl. J. Med. 349, 2014–2022 (2003).

  211. 211

    Gordon, K. B. et al. Clinical response to adalimumab treatment in patients with moderate to severe psoriasis: double-blind, randomized controlled trial and open-label extension study. J. Am. Acad. Dermatol. 55, 598–606 (2006).

  212. 212

    Mease, P. J. et al. Adalimumab for the treatment of patients with moderately to severely active psoriatic arthritis: results of a double-blind, randomized, placebo-controlled trial. Arthritis Rheum. 52, 3279–3289 (2005).

  213. 213

    Kavanaugh, A. et al. The Infliximab Multinational Psoriatic Arthritis Controlled Trial (IMPACT): results of radiographic analyses after 1 year. Ann. Rheum. Dis. 65, 1038–1043 (2006).

  214. 214

    Chaudhari, U. et al. Efficacy and safety of infliximab monotherapy for plaque-type psoriasis: a randomised trial. Lancet 357, 1842–1847 (2001).

  215. 215

    Gottlieb, A. B. et al. Infliximab induction therapy for patients with severe plaque-type psoriasis: a randomized, double-blind, placebo-controlled trial. J. Am. Acad. Dermatol. 51, 534–542 (2004).

  216. 216

    Salmon-Ceron, D. et al. Drug-specific risk of non-tuberculosis opportunistic infections in patients receiving anti-TNF therapy reported to the 3-year prospective French RATIO registry. Ann. Rheum. Dis. 70, 616–623 (2011).

  217. 217

    Reich, K. et al. Successful treatment of moderate to severe plaque psoriasis with the PEGylated Fab' certolizumab pegol: results of a phase II randomized, placebo-controlled trial with a re-treatment extension. Br. J. Dermatol. 167, 180–190 (2012).

  218. 218

    Mease, P. J. et al. Effect of certolizumab pegol on signs and symptoms in patients with psoriatic arthritis: 24-week results of a phase 3 double-blind randomised placebo-controlled study (RAPID-PsA). Ann. Rheum. Dis. 73, 48–55 (2014).

  219. 219

    Kavanaugh, A. et al. Golimumab in psoriatic arthritis: one-year clinical efficacy, radiographic, and safety results from a phase III, randomized, placebo-controlled trial. Arthritis Rheum. 64, 2504–2517 (2012).

  220. 220

    Langley, R. G. et al. Secukinumab in plaque psoriasis — results of two phase 3 trials. N. Engl. J. Med. 371, 326–338 (2014).

  221. 221

    Griffiths, C. E. et al. Comparison of ixekizumab with etanercept or placebo in moderate-to-severe psoriasis (UNCOVER-2 and UNCOVER-3): results from two phase 3 randomised trials. Lancet 386, 541–551 (2015).

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The authors acknowledge the late Dr T. Henseler for his pivotal early genetic and epidemiological research and his contribution to the psoriasis field.

Author information

Introduction (J.E.G. and A.B.G.); Epidemiology (J.J.W.); Mechanisms/pathophysiology (A.M.G. and A.B.G.); Diagnosis, screening and prevention (A.M.G., J.T.E., D.D.G. and N.N.M.); Management (M.G.L.); Quality of life (A.Y.F.); Outlook (J.E.G. and A.B.G.); Overview of Primer (A.B.G., J.E.G. and A.M.G.).

Correspondence to Alice B. Gottlieb.

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Competing interests

J.T.E. is currently serving as a scientific advisor for Janssen, a division of Johnson and Johnson. Since 2013 he has also served as a consultant or scientific advisor for Janssen, Novartis and Lilly and as a consultant for Pfizer. M.G.L. is an employee of Mount Sinai, which receives research funds from Amgen, Anacor, Boehringer Ingelheim, Celgene, Lilly, Janssen Biotech, Kadmon, LEO Pharmaceuticals, Medimmune, Novartis, Pfizer, Sun Pharmaceuticals and Valeant. D.D.G. has consulted and/or received grant support from AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Janssen, Novartis, Pfizer and UCB. J.J.W. has received research funding from AbbVie, Amgen, AstraZeneca, Boehringer Ingelheim, Coherus Biosciences, Dermira, Eli Lilly, Janssen, Merck, Novartis, Pfizer, Regeneron, Sandoz and Sun Pharmaceuticals; he is a consultant for AbbVie, Amgen, Celgene, Dermira, Eli Lilly, Pfizer, Regeneron, Sun Pharmaceuticals and Valeant Pharmaceuticals. All funds go to his employer. N.N.M. is a full-time US Government employee and Chief of the Section of Inflammation and Cardiometabolic Diseases at the National Heart, Lung, and Blood Institute. A.Y.F. has consultancy agreements with Novartis and received honoraria for advisory boards with Novartis, Galderma, Napp, Sanofi, Eli Lilly and Janssen, which funded a recent Cardiff University Dermatology Life Quality Index (DLQI) research project, in which he is a joint inventor and receives royalties. A.B.G. has current consulting and/or advisory board agreements: Amgen Inc., Astellas, Akros, Centocor (Janssen), Inc., Celgene Corp., Bristol-Myers Squibb Co., Beiersdorf, Inc., Abbott Labs (AbbVie), TEVA, Actelion, UCB, Novo Nordisk, Novartis, Dermipsor Ltd., Incyte, Pfizer, Canfite, Lilly, Coronado, Vertex, Karyopharm, CSL Behring Biotherapies for Life, GlaxoSmithKline, Xenoport, Catabasis, Meiji Seika Pharma Co., Ltd, Takeda, Mitsubishi, Tanabe Pharma Development America, Inc, Genentech, Baxalta, Kineta One, KPI Therapeutics, Crescendo Bioscience, Aclaris, Amicus, Reddy Labs. Research and/or educational grants (paid to Tufts Medical Center) until 5 November 2016, then none: Centocor (Janssen), Amgen, Abbott (AbbVie), Novartis, Celgene, Pfizer, Lilly, Levia, Merck, Xenoport, Dermira, Baxalta. J.E.G. and A.M.G. declare no competing interests.

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