title: Comparative analysis of circulating dendritic cell subsets in patients with atopic diseases and sarcoidosis.
abstract: BACKGROUND
  Dendritic cells (DCs) are professional antigen-presenting cells that play a crucial role in the initiation and modulation of immune responses. Human circulating blood DCs are divided into two major subsets: myeloid DCs (mDCs); and plasmacytoid DCs (pDCs). Furthermore, mDCs are subdivided into two subsets: Th1-promoting mDCs (mDC1s); and Th2-promoting mDCs (mDC2s). Although CD1a, CD1c, and CD141 are generally used for classifying mDC subsets, their adequacy as a specific marker remains unclear. We performed this study to compare circulating mDC, pDC, mDC1, and mDC2 subsets between Th1- and Th2-mediated diseases using CD1a and CD141, and to analyze the adequacy of CD1a and CD141 as a marker for mDC1s and mDC2s, respectively.
  
  
  METHODS
  Thirty patients with sarcoidosis, 23 patients with atopic diseases, such as atopic bronchial asthma, and 23 healthy subjects as controls were enrolled in this study. Peripheral blood DC subsets were analyzed with flow cytometry according to expressions of CD11c, CD123, CD1a, and CD141. For functional analysis, we measured interleukin (IL) 12p40 levels produced by the sorted mDC subsets.
  
  
  RESULTS
  The sarcoidosis group showed decreased total DC (P < 0.05) and mDC counts (P < 0.05) compared to controls. The atopy group showed decreased CD1a+mDC count (P < 0.05), and increased CD1a-mDC count (P < 0.05) compared to controls. CD141+mDC count in the atopy group was higher than controls (P < 0.05). Sorted CD1a+mDCs produced higher levels of IL-12p40 than CD1a-mDCs (P = 0.025) and CD141+mDCs (P = 0.018).
  
  
  CONCLUSIONS
  We conclude that decreased count of CD1a+mDC and increased count of CD141+mDC may reflect the Th2-skewed immunity in atopic diseases. The results of IL-12 levels produced by the sorted mDC subsets suggested the adequacy of CD1a and CD141 as a marker for mDC1 and mDC2, respectively, in vivo.
authors.affiliation: Department of Pulmonary Medicine and Clinical Immunology, Dokkyo Medical University, Kitakobayashi 880, Mibu, Tochigi, 321-0293, Japan.
authors.forename: Yumeko
authors.initials: Y
authors.lastname: Hayashi
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Ishii
authors.forename: Mitsumi
authors.initials: M
authors.lastname: Hata-Suzuki
authors.forename: Ryo
authors.initials: R
authors.lastname: Arai
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Chibana
authors.forename: Akihiro
authors.initials: A
authors.lastname: Takemasa
authors.forename: Takeshi
authors.initials: T
authors.lastname: Fukuda
mesh_terms: D000328:Adult; D000368:Aged; D001249:Asthma / Q000175:diagnosis / Q000453:epidemiology / Q000473:pathology*; D002465:Cell Movement / Q000276:immunology; D003713:Dendritic Cells / Q000378:metabolism* / Q000473:pathology; D003876:Dermatitis, Atopic / Q000175:diagnosis / Q000453:epidemiology / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012130:Respiratory Hypersensitivity / Q000175:diagnosis / Q000453:epidemiology / Q000473:pathology*; D012507:Sarcoidosis / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology