Regulation of T helper cell subsets by cyclooxygenases and their metabolites

Prostaglandins Other Lipid Mediat. 2013 Jul-Aug:104-105:74-83. doi: 10.1016/j.prostaglandins.2012.11.002. Epub 2012 Nov 28.

Abstract

Cyclooxygenases and their metabolites are important regulators of inflammatory responses and play critical roles in regulating the differentiation of T helper cell subsets in inflammatory diseases. In this review, we highlight new information on regulation of T helper cell subsets by cyclooxygenases and their metabolites. Prostanoids influence cytokine production by both antigen presenting cells and T cells to regulate the differentiation of naïve CD4(+) T cells to Th1, Th2 and Th17 cell phenotypes. Cyclooxygenases and PGE2 generally exacerbate Th2 and Th17 phenotypes, while suppressing Th1 differentiation. Thus, cycloxygenases may play a critical role in diseases that involve immune cell dysfunction. Targeting of cyclooxygenases and their eicosanoid products may represent a new approach for treatment of inflammatory diseases, tumors and autoimmune disorders.

Publication types

  • Review

MeSH terms

  • Autoimmune Diseases / drug therapy
  • Autoimmune Diseases / immunology
  • Autoimmune Diseases / metabolism*
  • Autoimmune Diseases / pathology
  • Cell Differentiation
  • Cyclooxygenase 2 / metabolism*
  • Cyclooxygenase Inhibitors / pharmacology
  • Cytokines / immunology
  • Cytokines / metabolism
  • Dinoprostone / metabolism*
  • Dinoprostone / pharmacology
  • Humans
  • Inflammation / drug therapy
  • Inflammation / immunology
  • Inflammation / metabolism
  • Inflammation / pathology
  • Th1 Cells / drug effects*
  • Th1 Cells / immunology
  • Th1 Cells / pathology
  • Th17 Cells / drug effects*
  • Th17 Cells / immunology
  • Th17 Cells / pathology
  • Th2 Cells / drug effects*
  • Th2 Cells / immunology
  • Th2 Cells / pathology

Substances

  • Cyclooxygenase Inhibitors
  • Cytokines
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Dinoprostone