title: Differential expression of toll-like receptor mRNAs in recurrent aphthous ulceration.
abstract: BACKGROUND
  Toll-like receptors (TLR) are membrane proteins that recognize conserved molecules derived from bacterial, viral, fungal or host tissues. They are responsible for promoting the production of cytokines and chemokines, increasing the expression of costimulatory molecules and influencing the T Helper response (Th) toward either a Th1 or Th2 profile, thereby modulating the regulatory T cell response and controlling the integrity of the epithelial barrier. The key factors responsible for increased susceptibility to recurrent aphthous ulceration (RAU) are unclear, and because TLRs are involved in both immune regulation and control of the epithelial barrier, a deficiency in TLR activity is likely to cause increased susceptibility.
  
  
  METHODS
  We investigated the gene expression of TLRs one through 10 in tissue samples and peripheral blood mononuclear cells (PBMC) of RAU patients in comparison to healthy controls using real-time quantitative reverse transcription PCR.
  
  
  RESULTS
  The analysis of mRNA expression levels in oral lesion showed significant (P < 0.01) overexpression of the TLR2 (~6-fold) gene and decreased expression of the TLR3 (~5-fold) and TLR5 (~6-fold) genes in comparison with healthy oral mucosa. The analysis of mRNA expression in PBMC indicated a down-regulation of TLR5 gene expression in the cells from RAU patients (P < 0.05; ~2-fold).
  
  
  CONCLUSIONS
  Our results support the hypothesis that a subset of RAU patients has fewer TLR expression that have been tentatively implicated in anti-inflammatory effects. This derangement of TLR gene expression may cause an overlay exuberant inflammation reaction in situations where normal individuals are resistant.
authors.affiliation: Discipline of Stomatology, School of Dentistry, University of Saõ Paulo, Saõ Paulo, Brazil.
authors.forename: Camila
authors.initials: C
authors.lastname: Gallo
authors.forename: Fabiana
authors.initials: F
authors.lastname: Barros
authors.forename: Norberto
authors.initials: N
authors.lastname: Sugaya
authors.forename: Fabio
authors.initials: F
authors.lastname: Nunes
authors.forename: Ricardo
authors.initials: R
authors.lastname: Borra
mesh_terms: D000293:Adolescent; D000328:Adult; D004198:Disease Susceptibility / Q000276:immunology; D015536:Down-Regulation / Q000276:immunology; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000032:analysis; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013281:Stomatitis, Aphthous / Q000276:immunology*; D051195:Toll-Like Receptor 2 / Q000032:analysis / Q000235:genetics; D051196:Toll-Like Receptor 3 / Q000032:analysis / Q000235:genetics; D051198:Toll-Like Receptor 5 / Q000032:analysis / Q000235:genetics; D051193:Toll-Like Receptors / Q000032:analysis* / Q000235:genetics; D055815:Young Adult
chemical_list: D012333:RNA, Messenger; C495342:TLR2 protein, human; C495344:TLR3 protein, human; C495346:TLR5 protein, human; D051195:Toll-Like Receptor 2; D051196:Toll-Like Receptor 3; D051198:Toll-Like Receptor 5; D051193:Toll-Like Receptors