Lipoteichoic acid downregulates FcepsilonRI expression on human mast cells through Toll-like receptor 2

J Allergy Clin Immunol. 2007 Aug;120(2):452-61. doi: 10.1016/j.jaci.2007.03.027. Epub 2007 May 3.


Background: FcepsilonRI on the surface of mast cells (MCs) plays a central role in allergic responses. Recent evidence shows that exposure to microbial components corresponds with a significant reduction in the risk for allergic diseases. Although many reports suggest that this is due to changes in T-cell functions, how MC functions are altered by bacterial infection remains unknown.

Objective: We sought to elucidate the effect of bacterial infection on MC function and expression of Fc receptors, such as FcepsilonRI.

Methods: Isolated human pulmonary MCs and a human MC line (LAD2) were stimulated with bacterial components, and the function and surface expression of Fc receptors were measured.

Results: Lipoteichoic acid (LTA) and peptidoglycan, but not LPS, flagellin, or 3CpG-oligodeoxynucleotide, reduced the expression of FcepsilonRI on LAD2 cells. An antibody to Toll-like receptor (TLR) 2 partially blocked the effect of LTA but not peptidoglycan. Both LTA and peptidoglycan reduced MC degranulation caused by an antigen-specific IgE. Furthermore, exposure of pulmonary MCs to LTA reduced both FcepsilonRI expression and IgE-induced degranulation. None of the bacterial components affected the expression of other Fc receptors, such as Fcgamma receptors or Fcalpha receptor I.

Conclusions: Our results indicate that LTA reduces the surface expression of FcepsilonRI through TLR2 and suggests that TLR2 ligands could be used as a novel therapy for controlling allergic disorders.

Clinical implications: By knowing how bacterial components modulate MC function, we can expand our possibilities for therapeutic interventions of allergic diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Degranulation / drug effects
  • Cell Line
  • Cell Membrane / metabolism
  • Dose-Response Relationship, Drug
  • Down-Regulation / physiology*
  • Humans
  • Ligands
  • Lipopolysaccharides / administration & dosage
  • Lipopolysaccharides / pharmacology*
  • Lung / cytology
  • Mast Cells / cytology
  • Mast Cells / metabolism*
  • Mast Cells / physiology
  • Peptidoglycan / administration & dosage
  • Peptidoglycan / pharmacology
  • RNA, Messenger / metabolism
  • Receptors, IgE / genetics
  • Receptors, IgE / metabolism*
  • Teichoic Acids / administration & dosage
  • Teichoic Acids / pharmacology*
  • Toll-Like Receptor 2 / physiology*
  • Toll-Like Receptors / metabolism


  • Ligands
  • Lipopolysaccharides
  • Peptidoglycan
  • RNA, Messenger
  • Receptors, IgE
  • Teichoic Acids
  • Toll-Like Receptor 2
  • Toll-Like Receptors
  • lipoteichoic acid