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This review gives an overview of the clinical picture, and characteristics of the patients as well as the diagnosis and therapy of EH. A special focus lies on the pathophysiological hallmarks identified so far that predispose for EH. This aspect covers genetic aberrations, immunological changes, and environmental influences displaying a complex multifactorial situation, which is not completely understood. Type 2 skewing of virus\u2010specific T cells in ADEH\n                    <jats:sup>+<\/jats:sup>\n                    patients has been implicated in immune profile abnormalities, along with impaired functions of dendritic cells and natural killer cells. Furthermore, aberrations in interferon pathway\u2010related genes such as\n                    <jats:italic>IFNG<\/jats:italic>\n                    and\n                    <jats:italic>IFNGR1<\/jats:italic>\n                    have been identified to increase the risk of EH. IL\u20104, IL\u201025, and thymic stromal lymphopoietin (TSLP) are overexpressed in EH, whereas antimicrobial peptides like human \u03b2\u2010defensins and LL\u201037 are reduced. Concerning the epidermal barrier, single nucleotide polymorphisms (SNPs) in skin barrier proteins such as filaggrin were identified in ADEH\n                    <jats:sup>+<\/jats:sup>\n                    patients. A dysbalance of the skin microbiome also contributes to EH due to an increase of\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    , which provides a supporting role to the viral infection via secreted toxins such as \u03b1\u2010toxin. The risk of EH is reduced in AD patients treated with dupilumab. Further research is needed to identify and specifically target risk factors for EH in AD patients.\n                  <\/jats:p>","DOI":"10.1111\/all.14853","type":"journal-article","created":{"date-parts":[[2021,4,12]],"date-time":"2021-04-12T12:59:41Z","timestamp":1618232381000},"page":"3017-3027","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":104,"title":["Eczema herpeticum in atopic dermatitis"],"prefix":"10.1111","volume":"76","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4806-599X","authenticated-orcid":false,"given":"Stephan","family":"Traidl","sequence":"first","affiliation":[{"name":"Division of Immunodermatology and Allergy Research Department of Dermatology and Allergy Hannover Medical School Hannover Germany"},{"name":"Cluster of Excellence RESIST (EXC 2155) Hannover Medical School Hannover Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6651-0458","authenticated-orcid":false,"given":"Lennart","family":"Roesner","sequence":"additional","affiliation":[{"name":"Division of Immunodermatology and Allergy Research Department of Dermatology and Allergy Hannover Medical School Hannover Germany"},{"name":"Cluster of Excellence RESIST (EXC 2155) Hannover Medical School Hannover Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jana","family":"Zeitvogel","sequence":"additional","affiliation":[{"name":"Division of Immunodermatology and Allergy Research Department of Dermatology and Allergy Hannover Medical School Hannover Germany"},{"name":"Cluster of Excellence RESIST (EXC 2155) Hannover Medical School Hannover Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Werfel","sequence":"additional","affiliation":[{"name":"Division of Immunodermatology and Allergy Research Department of Dermatology and Allergy Hannover Medical School Hannover Germany"},{"name":"Cluster of Excellence RESIST (EXC 2155) Hannover Medical School Hannover Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2021,5,3]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaci.2016.06.010"},{"key":"e_1_2_11_3_1","unstructured":"WillanR.On cutaneous diseases. 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