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The aetiology of psoriasis is thought to originate from an interplay of genetic, environmental, infectious and lifestyle factors. The manner in which genetic and environmental factors interact to contribute to the molecular disease mechanisms has remained elusive. However, the interleukin 23 (\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201023)\/T\u2010helper 17 (\n                    <jats:styled-content style=\"fixed-case\">\n                      T\n                      <jats:sub>H<\/jats:sub>\n                    <\/jats:styled-content>\n                    17) immune axis has been identified as a major immune pathway in psoriasis disease pathogenesis. Central to this pathway is the cytokine\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201023, a heterodimer composed of a p40 subunit also found in\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201012 and a p19 subunit exclusive to\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201023.\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201023 is important for maintaining\n                    <jats:styled-content style=\"fixed-case\">\n                      T\n                      <jats:sub>H<\/jats:sub>\n                    <\/jats:styled-content>\n                    17 responses, and levels of\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201023 are elevated in psoriatic skin compared with non\u2010lesional skin. A number of agents that specifically inhibit\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201023p19 are currently in development for the treatment of moderate\u2010to\u2010severe plaque psoriasis, with recent clinical trials demonstrating efficacy with a good safety and tolerability profile. These data support the role of this cytokine in the pathogenesis of psoriasis. A better understanding of the\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201023\/\n                    <jats:styled-content style=\"fixed-case\">\n                      T\n                      <jats:sub>H<\/jats:sub>\n                    <\/jats:styled-content>\n                    17 immune axis is vital and will promote the development of additional targets for psoriasis and other inflammatory diseases that share similar genetic aetiology and pathogenetic pathways.\n                  <\/jats:p>","DOI":"10.1111\/jdv.14433","type":"journal-article","created":{"date-parts":[[2017,6,27]],"date-time":"2017-06-27T01:54:47Z","timestamp":1498528487000},"page":"1616-1626","source":"Crossref","is-referenced-by-count":306,"title":["The role of\n                    <scp>IL<\/scp>\n                    \u201023 and the\n                    <scp>IL<\/scp>\n                    \u201023\/\n                    <scp>\n                      T\n                      <sub>H<\/sub>\n                    <\/scp>\n                    17 immune axis in the pathogenesis and treatment of psoriasis"],"prefix":"10.1111","volume":"31","author":[{"given":"G.","family":"Girolomoni","sequence":"first","affiliation":[{"name":"Section of Dermatology Department of Medicine University of Verona Verona Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Strohal","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Venerology Federal Academic Teaching Hospital of Feldkirch Feldkirch Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L.","family":"Puig","sequence":"additional","affiliation":[{"name":"Hospital de la Santa Creu i Sant Pau Universitat Aut\u00f2noma de Barcelona Barcelona Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.","family":"Bachelez","sequence":"additional","affiliation":[{"name":"Sorbonne Paris Cit\u00e9 Universit\u00e9 Paris Diderot Paris France"},{"name":"Department of Dermatology H\u00f4pital Saint\u2010Louis Assistance Publique\u2010H\u00f4pitaux de Paris (AP\u2010HP) Paris France"},{"name":"UMR INSERM U1163 Institut Imagine Paris France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Barker","sequence":"additional","affiliation":[{"name":"St John's Institute of Dermatology King's College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W.H.","family":"Boehncke","sequence":"additional","affiliation":[{"name":"Division of Dermatology Geneva University Hospitals Department of Pathology and Immunology Faculty of Medicine University of Geneva Geneva Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.C.","family":"Prinz","sequence":"additional","affiliation":[{"name":"Department of Dermatology University of Munich Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,8,29]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaut.2005.09.025"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(14)61909-7"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaut.2015.07.008"},{"key":"e_1_2_7_5_1","unstructured":"World Health Organization.Global Report in Psoriasis.2016."},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2133.2010.10134.x"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1038\/jid.2013.446"},{"key":"e_1_2_7_8_1","unstructured":"National Psoriasis Foundation.Plaque Psoriasis.2016. 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