title: Advances in atopic dermatitis in 2015.
abstract: This review aims to highlight recently published articles on atopic dermatitis (AD). Updated are the insights into epidemiology, pathology, diagnostics, and therapy. Epidemiologic studies have revealed a positive correlation between AD and systemic conditions, such as rheumatoid arthritis, inflammatory bowel disease, and neonatal adiposity. Pathologic findings highlight the involvement of novel barrier factors (desmoplakin and claudin), novel immune cell subsets (pathogenic effector TH2 cells and group 2 innate lymphoid cells), and differential skewing of helper T cells (eg, TH17 dominance in Asians with AD). As diagnostics, noninvasive examinations of the transepidermal water loss of neonates, the density of epidermal Staphylococcus species, and the gut flora might prognosticate the onset of AD. As for therapy, various methods are proposed, including conventional (petrolatum and UV) and molecule-oriented regimens targeting Janus kinase, signal transducer and activator of transcription 3, extracellular signal-regulated kinase, sirtuin 1, or aryl hydrocarbon receptor.
authors.affiliation: Department of Dermatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Department of Experimental Therapeutics, Institute for Advancement of Clinical and Translational Science (iACT), Kyoto University Hospital, Kyoto, Japan. Electronic address: tnomura@kuhp.kyoto-u.ac.jp.
authors.forename: Takashi
authors.initials: T
authors.lastname: Nomura
authors.affiliation: Department of Dermatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Singapore Immunology Network (SIgN) and Institute of Medical Biology, Agency for Science, Technology and Research (A*STAR), Biopolis, Singapore; PRESTO, Japan Science and Technology Agency, Saitama, Japan.
authors.forename: Kenji
authors.initials: K
authors.lastname: Kabashima
mesh_terms: D000818:Animals; D001172:Arthritis, Rheumatoid / Q000453:epidemiology*; D057167:Claudins / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000175:diagnosis / Q000188:drug therapy / Q000453:epidemiology*; D051180:Desmoplakins / Q000378:metabolism; D000091344:Filaggrin Proteins; D006801:Humans; D007113:Immunity, Innate; D007231:Infant, Newborn; D015212:Inflammatory Bowel Diseases / Q000453:epidemiology*; D053612:Janus Kinases / Q000378:metabolism; D058990:Molecular Targeted Therapy; D009765:Obesity / Q000453:epidemiology*; D013203:Staphylococcal Infections / Q000453:epidemiology*; D013210:Staphylococcus / Q000502:physiology*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D057167:Claudins; D051180:Desmoplakins; C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D053612:Janus Kinases
keywords: Atopic dermatitis; JTE-052; Janus kinase; T(H)1; T(H)17; T(H)2; T(H)22; adiposity; aryl hydrocarbon receptor; biologics; chemoattractant receptor-homologous molecule expressed on T(H)2 cells; chemokines; cytokines; extracellular signal-regulated kinase; filaggrin; pathogenic effector T(H)2; petrolatum; signal transducer and activator of transcription 3; sirtuin 1; thymic stromal lymphopoietin; transepidermal water loss; ultraviolet B