title: Increased expression of CC chemokine ligand 18 in extrinsic atopic dermatitis patients.
abstract: BACKGROUND
  Although most patients with atopic dermatitis (AD) show high total and allergen-specific serum immunoglobulin E (IgE) levels, a small subgroup of AD patients have normal total IgE levels and negative serum allergen-specific IgE. This subgroup has been termed 'intrinsic' AD (IAD) as a counterpart to 'extrinsic' AD (EAD). However, the difference of chemokines between IAD and EAD has not yet been evaluated.
  
  
  OBJECTIVE
  We investigated the expression of CC chemokine ligand (CCL) 17, CCL22, and CCL18 in patients with IAD and EAD, which are known to be highly expressed in AD patients.
  
  
  METHODS
  We assessed the protein levels of these chemokines in peripheral blood mononuclear cells (PBMCs), sera and lesional skins. We also evaluated CCL18 mRNA levels in monocytes, Langerhans cell (LC)-like dendritic cells (DCs) and inflammatory dendritic epidermal cell (IDEC)-like DCs from both types of AD patients.
  
  
  RESULTS
  There were no significant differences in CCL17 and CCL22 expression in PBMCs, sera and lesional skins of patients with IAD and EAD. CCL18 expression did not differ in PBMCs, sera and LC-like DCs from the two subgroups, but strong CCL18 expression was observed in lesional skins and IDEC-like DCs in patients with EAD. Lastly, serum CCL18 levels significantly decreased after immunotherapy.
  
  
  CONCLUSIONS
  This study suggests that the chemokine micromilieu, especially the level of CCL18, is different between EAD and IAD patients. High FcepsilonRI surface-expressing DCs, such as IDEC, were the major source of CCL18, and produced a prominent CCL18 microenvironment in EAD patients compared with IAD patients.
authors.affiliation: Department of Dermatology, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Chang Ook
authors.initials: CO
authors.lastname: Park
authors.forename: Hee Jung
authors.initials: HJ
authors.lastname: Lee
authors.forename: Ju Hee
authors.initials: JH
authors.lastname: Lee
authors.forename: Wen Hao
authors.initials: WH
authors.lastname: Wu
authors.forename: Nam Soo
authors.initials: NS
authors.lastname: Chang
authors.forename: Liu
authors.initials: L
authors.lastname: Hua
authors.forename: Min-Geol
authors.initials: MG
authors.lastname: Lee
authors.forename: Kwang Hoon
authors.initials: KH
authors.lastname: Lee
mesh_terms: D000293:Adolescent; D000328:Adult; D001706:Biopsy; D016022:Case-Control Studies; D002478:Cells, Cultured; D054414:Chemokine CCL17 / Q000378:metabolism; D054422:Chemokine CCL22 / Q000378:metabolism; D019742:Chemokines, CC / Q000378:metabolism*; D002648:Child; D003876:Dermatitis, Atopic / Q000145:classification* / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007801:Langerhans Cells / Q000378:metabolism / Q000473:pathology; D008297:Male; D009000:Monocytes / Q000378:metabolism / Q000473:pathology; D012867:Skin / Q000378:metabolism* / Q000473:pathology
chemical_list: C106230:CCL17 protein, human; C111792:CCL18 protein, human; C515482:CCL22 protein, human; D054414:Chemokine CCL17; D054422:Chemokine CCL22; D019742:Chemokines, CC; D007073:Immunoglobulin E