Negative feedback regulation of T helper type 1 (Th1)/Th2 cytokine balance via dendritic cell and natural killer T cell interactions

Blood. 2005 Sep 1;106(5):1685-93. doi: 10.1182/blood-2004-12-4738. Epub 2005 May 5.

Abstract

The ability of extracellular stimuli to modulate dendritic cell (DC) activation of natural killer T (NKT) cells was not well understood. We investigated the effects of the T helper type 1 (Th1)/Th2-cytokine environment on DC induction of NKT cell-mediated cytokine production in mice. Pretreatment of myeloid DCs with Th1 or Th2 cytokines, interleukin (IL)-4 or interferon (IFN)-gamma, led to the enhanced production of reciprocal cytokines by NKT cells (eg, IL-4 pretreatment led to the enhanced production of Th1 cytokines) in vitro and in vivo. Thus, the recognition of Th1 or Th2 cytokines by DCs acts as a negative feedback loop to maintain Th1/Th2-cytokine balance via NKT cell functions. Using these data, we manipulated cytokine levels and innate cytolytic activity in vivo to increase an antitumor response. This is the first description of a novel regulation system governing Th1/Th2 cytokine balance involving DCs and NKT cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Communication / immunology
  • Cell Differentiation / drug effects
  • Cell Differentiation / physiology
  • Cytokines / biosynthesis
  • Cytokines / immunology*
  • Cytokines / pharmacology
  • Dendritic Cells / drug effects
  • Dendritic Cells / immunology*
  • Feedback, Physiological*
  • Female
  • Flow Cytometry
  • Interferon-gamma / analysis
  • Interferon-gamma / immunology
  • Interferon-gamma / pharmacology
  • Interleukin-12 / biosynthesis
  • Interleukin-4 / analysis
  • Interleukin-4 / immunology
  • Interleukin-4 / pharmacology
  • Killer Cells, Natural / drug effects
  • Killer Cells, Natural / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Sulfoglycosphingolipids / pharmacology
  • Th1 Cells / immunology*
  • Th2 Cells / immunology*

Substances

  • Cytokines
  • Sulfoglycosphingolipids
  • Interleukin-12
  • Interleukin-4
  • Interferon-gamma