title: Major differences in inflammatory dendritic cells and their products distinguish atopic dermatitis from psoriasis.
abstract: BACKGROUND
  Atopic dermatitis (AD) and psoriasis represent contrasting poles of the T(H)1 versus T(H)2 paradigm. Both diseases have been associated with increased numbers of dendritic cells (DCs) in the skin, but the similarities and differences in DC populations need to be established.
  
  
  OBJECTIVE
  We aimed to characterize the specific DC subsets, as well as chemokine and cytokine environment in chronic AD compared with psoriasis.
  
  
  METHODS
  Skin biopsies were obtained from patients with acute exacerbation of chronic AD (n = 18), psoriasis (n = 15), and healthy volunteers (n = 15) for microarray analysis, RT-PCR, immunohistochemistry, and double-label immunofluorescence.
  
  
  RESULTS
  Myeloid DCs upregulate CCL17 and CCL18 in AD, as opposed to TNF-alpha and inducible nitric oxide synthase (iNOS) in psoriasis. In our study, we identified cells phenotypically identical to the inflammatory dendritic epidermal cells in the dermis in both diseases, although to a lesser extent in psoriasis. We found substantially higher numbers of dermal CCL22 producing plasmacytoid DCs in AD. The thymic stromal lymphopoietin receptor showed significantly higher expression in AD, whereas the thymic stromal lymphopoietin ligand was upregulated more in psoriasis.
  
  
  CONCLUSIONS
  There are major differences in myeloid and plasmacytoid subsets of cutaneous DCs and the chemokine/cytokine environment between AD and psoriasis. Distinct subsets within the CD11c(+) population may influence polarization through the production of regulatory mediators, including iNOS, TNF, CCL17, and CCL18. Plasmacytoid DCs may also influence T(H)2 polarization, having a more important role in AD than previously appreciated.
  
  
  CONCLUSIONS
  Dermal inflammatory dendritic cells in AD and TNF and iNOS-producing DCs in psoriasis, and/or their regulatory products, may be potential targets for future therapeutic interventions.
authors.affiliation: Laboratory for Investigative Dermatology, Rockefeller University, New York, NY 10021, USA.
authors.forename: Emma
authors.initials: E
authors.lastname: Guttman-Yassky
authors.forename: Michelle A
authors.initials: MA
authors.lastname: Lowes
authors.forename: Judilyn
authors.initials: J
authors.lastname: Fuentes-Duculan
authors.forename: Julia
authors.initials: J
authors.lastname: Whynot
authors.forename: Inna
authors.initials: I
authors.lastname: Novitskaya
authors.forename: Irma
authors.initials: I
authors.lastname: Cardinale
authors.forename: Asifa
authors.initials: A
authors.lastname: Haider
authors.forename: Artemis
authors.initials: A
authors.lastname: Khatcherian
authors.forename: John A
authors.initials: JA
authors.lastname: Carucci
authors.forename: Reuven
authors.initials: R
authors.lastname: Bergman
authors.forename: James G
authors.initials: JG
authors.lastname: Krueger
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D016207:Cytokines / Q000096:biosynthesis; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000276:immunology*; D005260:Female; D005455:Fluorescent Antibody Technique; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D020411:Oligonucleotide Array Sequence Analysis; D011565:Psoriasis / Q000276:immunology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012867:Skin / Q000166:cytology / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D016207:Cytokines