Notch simultaneously orchestrates multiple helper T cell programs independently of cytokine signals

Immunity. 2013 Jul 25;39(1):148-59. doi: 10.1016/j.immuni.2013.07.006.

Abstract

Two models are proposed to explain Notch function during helper T (Th) cell differentiation. One argues that Notch instructs one Th cell fate over the other, whereas the other posits that Notch function is dictated by cytokines. Here we provide a detailed mechanistic study investigating the role of Notch in orchestrating Th cell differentiation. Notch neither instructed Th cell differentiation nor did cytokines direct Notch activity, but instead, Notch simultaneously regulated the Th1, Th2, and Th17 cell genetic programs independently of cytokine signals. In addition to regulating these programs in both polarized and nonpolarized Th cells, we identified Ifng as a direct Notch target. Notch bound the Ifng CNS-22 enhancer, where it synergized with Tbet at the promoter. Thus, Notch acts as an unbiased amplifier of Th cell differentiation. Our data provide a paradigm for Notch in hematopoiesis, with Notch simultaneously orchestrating multiple lineage programs, rather than restricting alternate outcomes.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Base Sequence
  • Cells, Cultured
  • Cytokines / immunology*
  • Cytokines / metabolism
  • Flow Cytometry
  • Gene Expression / immunology
  • Host-Parasite Interactions / immunology
  • Interferon-gamma / genetics
  • Interferon-gamma / immunology
  • Interferon-gamma / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Molecular Sequence Data
  • Protein Binding / immunology
  • Receptor, Notch1 / immunology*
  • Receptor, Notch1 / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sequence Homology, Nucleic Acid
  • Signal Transduction / immunology*
  • Th1 Cells / immunology*
  • Th1 Cells / metabolism
  • Th1 Cells / parasitology
  • Th17 Cells / immunology*
  • Th17 Cells / metabolism
  • Th2 Cells / immunology*
  • Th2 Cells / metabolism
  • Trichuris / immunology
  • Trichuris / physiology

Substances

  • Cytokines
  • Notch1 protein, mouse
  • Receptor, Notch1
  • Interferon-gamma