LPS-activated monocytes suppress T-cell immune responses and induce FOXP3+ T cells through a COX-2-PGE2-dependent mechanism

Int Immunol. 2008 Feb;20(2):235-45. doi: 10.1093/intimm/dxm134. Epub 2007 Dec 20.

Abstract

Monocytes initiate innate immune responses and interact with T cells to induce antigen-specific immune responses by antigen presentation and secretion of humoral factors. We have previously shown that adaptive regulatory T cells inhibit T-cell effector functions in a cyclooxygenase (COX)-2-prostaglandin E(2) (PGE(2))-dependent manner and that PGE(2) converts resting CD4+CD25- T cells into FOXP3+ T cells with a suppressive phenotype. Here, we demonstrate that stimulation of monocytes with LPS leads to suppression of T-cell immune responses by a COX-2-PGE(2)-dependent mechanism that is reversible with COX-2 inhibitors as well as PGE(2)-neutralizing antibody and cAMP antagonist. Furthermore, we show that LPS-activated monocytes induce FOXP3 expression in resting CD4+CD25- T cells by the same pathway. These results suggest that monocytes are able to efficiently suppress T-cell immune responses in a regulatory manner and elicit an inhibitory immune profile.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / metabolism
  • Cell Communication / immunology
  • Cyclooxygenase 2 / metabolism*
  • Cytokines / metabolism
  • Dinoprostone / metabolism*
  • Forkhead Transcription Factors / metabolism*
  • Humans
  • Interleukin-2 Receptor alpha Subunit / deficiency
  • Lipopolysaccharides / pharmacology*
  • Lymphocyte Activation / immunology
  • Monocytes / immunology*
  • T-Lymphocytes / immunology*

Substances

  • Cytokines
  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • Interleukin-2 Receptor alpha Subunit
  • Lipopolysaccharides
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Dinoprostone