Cutting edge: Genetic variation in TLR1 is associated with Pam3CSK4-induced effector T cell resistance to regulatory T cell suppression

J Immunol. 2014 Dec 15;193(12):5786-90. doi: 10.4049/jimmunol.1401185. Epub 2014 Nov 5.

Abstract

TLR play essential roles in the initiation and modulation of immune responses. TLR1/TLR2 heterodimers recognize triacylated bacterial lipopeptides, including the synthetic TLR1/2 lipopeptide Pam3CSK4. Genetic variation in TLR1 is associated with outcomes in diseases in which regulatory T cells (Treg) play a role, including asthma and allergy. To determine whether genetic polymorphisms in TLR1 are associated with alterations in Treg suppression of effector T cells (Teff), we performed in vitro suppression assays in healthy individuals with various haplotypes in TLR1. We show that functional genetic polymorphisms in TLR1 modify surface expression of TLR1 on T lymphocytes and confer enhanced Teff resistance to Treg suppression in the presence of Pam3CSK4. These effects are mediated, in part, by IL-6 and inhibited by blocking IL-6 signaling through STAT3. These findings suggest that TLR1 polymorphisms could influence immune-related disease through Teff resistance to Treg suppression.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Cell Membrane / metabolism
  • Genetic Variation*
  • Haplotypes
  • Humans
  • Immunomodulation / genetics
  • Interleukin-6 / biosynthesis
  • Lipopeptides / pharmacology
  • Polymorphism, Single Nucleotide
  • STAT3 Transcription Factor / antagonists & inhibitors
  • T-Lymphocyte Subsets / drug effects
  • T-Lymphocyte Subsets / immunology*
  • T-Lymphocyte Subsets / metabolism*
  • T-Lymphocytes, Regulatory / immunology*
  • T-Lymphocytes, Regulatory / metabolism
  • Toll-Like Receptor 1 / genetics*
  • Toll-Like Receptor 1 / metabolism*

Substances

  • Interleukin-6
  • Lipopeptides
  • Pam(3)CSK(4) peptide
  • STAT3 Transcription Factor
  • Toll-Like Receptor 1