title: Differential expression of toll-like receptor 2 on dendritic cells from asymptomatic and symptomatic atopic donors.
abstract: BACKGROUND
  Early microbial exposure may reduce the risk for developing allergies on an atopic genetic background. Toll-like receptors (TLRs) recognize pathogen-associated molecular patterns of microbes and modulate innate and adaptive immunity. Different expression of TLRs in symptomatic and asymptomatic atopic donors may contribute to the development of allergic disease.
  
  
  METHODS
  Monocytes and monocyte-derived dendritic cells (DCs) from symptomatic (n = 12) and asymptomatic atopic donors (n = 11), healthy nonatopics (n = 14) and from patients with psoriasis (n = 13) were analyzed for their expression of TLR2, TLR4 and TLR9 by real-time PCR.
  
  
  RESULTS
  Monocytes did not show any differences in TLR2, TLR4 and TLR9 expression between the 4 groups. In contrast, DCs from asymptomatic donors showed an enhanced expression of TLR2 over DCs from nonatopics (p = 0.038) and just failed to reach significance when compared to symptomatic atopic patients (p = 0.060). TLR2 expression kinetics from monocytes to monocyte-derived DCs showed sustained expression of TLR2 in DCs only from asymptomatic donors but downregulation in the other groups. In DCs from symptomatic atopic donors, the expression of TLR2 correlated significantly with total IgE values in the serum (p = 0.01994).
  
  
  CONCLUSIONS
  Differential expression and functional regulation of TLR2 expression by DCs from symptomatic and asymptomatic atopic donors may be important for the manifestation of allergic disease. Increased and sustained TLR2 expression on DCs, possibly as a result of an increased exposure to microorganisms or as a mechanism enhancing the sensitivity of microbe detection, may be of functional importance for the maintenance of clinical unresponsiveness toward allergens.
authors.affiliation: Department of Dermatology and Allergology, University of Bonn, Bonn, Germany. d.bubnoff@uni-bonn.de
authors.forename: D
authors.initials: D
authors.lastname: von Bubnoff
authors.forename: U
authors.initials: U
authors.lastname: Sell
authors.forename: S
authors.initials: S
authors.lastname: Arriens
authors.forename: S
authors.initials: S
authors.lastname: Specht
authors.forename: A
authors.initials: A
authors.lastname: Hoerauf
authors.forename: T
authors.initials: T
authors.lastname: Bieber
mesh_terms: D000293:Adolescent; D000328:Adult; D000485:Allergens / Q000276:immunology; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000276:immunology*; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D007073:Immunoglobulin E / Q000097:blood; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D011565:Psoriasis / Q000276:immunology; D012333:RNA, Messenger / Q000276:immunology; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000276:immunology*; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000276:immunology; D051217:Toll-Like Receptor 9 / Q000235:genetics / Q000276:immunology; D055815:Young Adult
chemical_list: D000485:Allergens; D012333:RNA, Messenger; C495342:TLR2 protein, human; C495345:TLR4 protein, human; C495371:TLR9 protein, human; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051217:Toll-Like Receptor 9; D007073:Immunoglobulin E