title: Toll-like receptor 2 is highly expressed in lesions of acne inversa and colocalizes with C-type lectin receptor.
abstract: BACKGROUND
  Acne inversa (hidradenitis suppurativa) is a chronic inflammatory and cicatricial disorder that affects skin areas rich in apocrine glands and terminal hairs, such as perineum and axillae. The exact pathogenesis of the disease is not well understood and the mechanisms by which bacterial superinfection contributes to the disease progression are not clear. Toll-like receptors (TLRs) expressed by inflammatory cells play a crucial role in the innate immune response to bacteria.
  
  
  OBJECTIVE
  We sought to investigate the role of TLR2 in the pathogenesis of acne inversa.
  
  
  METHODS
  We investigated the expression of TLR2 using real-time polymerase chain reaction analysis and immunohistochemical stainings of tissue samples from patients with acne inversa. Furthermore, we phenotypically characterized the infiltrating cells and their expression of TLR2.
  
  
  RESULTS
  Compared with normal skin, a highly increased in situ expression of TLR2 in acne inversa skin lesions was found at both the mRNA and the protein level. The most abundant cells in the dermal infiltrate of acne inversa were CD68+ macrophages, CD209+ dendritic cells (DCs) and CD3+ T cells. CD19+ B cells and CD56+ natural killer cells were found only in small numbers. Double staining with fluorescence-labelled antibodies showed that TLR2 was expressed by infiltrating macrophages (CD68+) and DCs (CD209+). Flow cytometric analysis of isolated infiltrating cells further confirmed surface expression of TLR2 by macrophages and DCs.
  
  
  CONCLUSIONS
  These data indicate that the enhanced expression of TLR2 by infiltrating macrophages and DCs may contribute to the pathogenesis of inflammatory lesions of acne inversa.
authors.affiliation: Department of Dermatology, University of Bern, Inselspital, 3010 Bern, Switzerland. robert.hunger@insel.ch
authors.forename: R E
authors.initials: RE
authors.lastname: Hunger
authors.forename: A M
authors.initials: AM
authors.lastname: Surovy
authors.forename: A S
authors.initials: AS
authors.lastname: Hassan
authors.forename: L R
authors.initials: LR
authors.lastname: Braathen
authors.forename: N
authors.initials: N
authors.lastname: Yawalkar
mesh_terms: D000328:Adult; D000368:Aged; D018076:DNA, Complementary / Q000302:isolation & purification; D005260:Female; D005434:Flow Cytometry / Q000379:methods*; D005455:Fluorescent Antibody Technique; D015870:Gene Expression; D017497:Hidradenitis Suppurativa / Q000209:etiology* / Q000378:metabolism; D006801:Humans; D037181:Lectins, C-Type / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D016133:Polymerase Chain Reaction / Q000379:methods; D012313:RNA / Q000302:isolation & purification; D012867:Skin / Q000378:metabolism* / Q000473:pathology; D051195:Toll-Like Receptor 2 / Q000378:metabolism*
chemical_list: D018076:DNA, Complementary; D037181:Lectins, C-Type; D051195:Toll-Like Receptor 2; D012313:RNA