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Debate remains over whether <jats:styled-content style=\"fixed-case\">DN<\/jats:styled-content> represent progressive lesions from <jats:styled-content style=\"fixed-case\">CMN<\/jats:styled-content>. Through gene expression profiling and analysis of molecular gene signatures, our study revealed progressive increases in immune activation and regulation, along with pathways implicated in melanomagenesis, from <jats:styled-content style=\"fixed-case\">CMN<\/jats:styled-content> to <jats:styled-content style=\"fixed-case\">DN<\/jats:styled-content> to <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content>. Using criteria of 1.5\u2010fold change and false discovery rate \u22640.05, we found differential expression of 7186 probes (6370 unique genes) with the largest difference detected between <jats:styled-content style=\"fixed-case\">DN<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content> from the standpoint of genomic melanoma progression. Despite progressive increases in the T\u2010helper type 1 (Th1)\u2010inducing gene (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201012), <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> indicated impaired Th1 or cytotoxic T\u2010cell response (decreased <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3) in <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content>. Concordantly, our results indicated progressive increases in molecular markers associated with regulatory T cells, exhausted T cells and tolerogenic dendritic cells, including detection of increased expression of suppressor of cytokine signalling 3 (<jats:styled-content style=\"fixed-case\">SOCS<\/jats:styled-content>3) in dendritic cells associated with <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content>. All together, our findings suggest that the increased immunosuppressive microenvironment of melanoma may contribute to unhampered proliferation of neoplastic cells. In addition, the detection of increased markers associated with tolerogenic dendritic cells in <jats:styled-content style=\"fixed-case\">MM<\/jats:styled-content> suggests that targeting these suppressive immune cell types may represent an alternative avenue for future immunotherapy.<\/jats:p>","DOI":"10.1111\/exd.13805","type":"journal-article","created":{"date-parts":[[2018,10,16]],"date-time":"2018-10-16T17:32:46Z","timestamp":1539711166000},"page":"35-44","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Novel immune signatures associated with dysplastic naevi and primary cutaneous melanoma in human skin"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8302-5104","authenticated-orcid":false,"given":"Bernice Y.","family":"Yan","sequence":"first","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University  New York City New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandra","family":"Garcet","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University  New York City New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas","family":"Gulati","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University  New York City New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Felix","family":"Kiecker","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Allergy Skin Cancer Center Charit\u00e9 Universit\u00e4tsmedizin Berlin  Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8022-1302","authenticated-orcid":false,"given":"Judilyn","family":"Fuentes\u2010Duculan","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University  New York City New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patricia","family":"Gilleaudeau","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University  New York City New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary","family":"Sullivan\u2010Whalen","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University  New York City New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Avner","family":"Shemer","sequence":"additional","affiliation":[{"name":"Department of Dermatology Tel\u2010Hashomer Medical Center  Ramat Gan Israel"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroshi","family":"Mitsui","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University  New York City New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James G.","family":"Krueger","sequence":"additional","affiliation":[{"name":"Laboratory for Investigative Dermatology The Rockefeller University  New York City New York"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2018,12,21]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/modpathol.3800515"},{"issue":"42","key":"e_1_2_8_3_1","first-page":"2010","volume":"141","author":"Bergman W.","year":"1997","journal-title":"Ned. 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