Dll4-Notch signaling in Flt3-independent dendritic cell development and autoimmunity in mice

J Exp Med. 2012 May 7;209(5):1011-28. doi: 10.1084/jem.20111615. Epub 2012 Apr 30.

Abstract

Delta-like ligand 4 (Dll4)-Notch signaling is essential for T cell development and alternative thymic lineage decisions. How Dll4-Notch signaling affects pro-T cell fate and thymic dendritic cell (tDC) development is unknown. We found that Dll4 pharmacological blockade induces accumulation of tDCs and CD4(+)CD25(+)FoxP3(+) regulatory T cells (T(reg) cells) in the thymic cortex. Both genetic inactivation models and anti-Dll4 antibody (Ab) treatment promote de novo natural T(reg) cell expansion by a DC-dependent mechanism that requires major histocompatibility complex II expression on DCs. Anti-Dll4 treatment converts CD4(-)CD8(-)c-kit(+)CD44(+)CD25(-) (DN1) T cell progenitors to immature DCs that induce ex vivo differentiation of naive CD4(+) T cells into T(reg) cells. Induction of these tolerogenic DN1-derived tDCs and the ensuing expansion of T(reg) cells are Fms-like tyrosine kinase 3 (Flt3) independent, occur in the context of transcriptional up-regulation of PU.1, Irf-4, Irf-8, and CSF-1, genes critical for DC differentiation, and are abrogated in thymectomized mice. Anti-Dll4 treatment fully prevents type 1 diabetes (T1D) via a T(reg) cell-mediated mechanism and inhibits CD8(+) T cell pancreatic islet infiltration. Furthermore, a single injection of anti-Dll4 Ab reverses established T1D. Disease remission and recurrence are correlated with increased T(reg) cell numbers in the pancreas-draining lymph nodes. These results identify Dll4-Notch as a novel Flt3-alternative pathway important for regulating tDC-mediated T(reg) cell homeostasis and autoimmunity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing
  • Amyloid Precursor Protein Secretases / deficiency
  • Amyloid Precursor Protein Secretases / metabolism
  • Animals
  • Antibodies / pharmacology
  • Blotting, Western
  • Calcium-Binding Proteins
  • Cell Differentiation / immunology*
  • DNA Primers / genetics
  • Dendritic Cells / immunology
  • Dendritic Cells / physiology*
  • Diabetes Mellitus, Type 1 / immunology
  • Diabetes Mellitus, Type 1 / prevention & control*
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • Fluorescent Antibody Technique
  • Genes, MHC Class II / immunology
  • Intracellular Signaling Peptides and Proteins / immunology
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Membrane Glycoproteins / deficiency
  • Membrane Glycoproteins / metabolism
  • Membrane Proteins / immunology
  • Membrane Proteins / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred NOD
  • Mice, Transgenic
  • Microscopy, Confocal
  • Oligonucleotide Array Sequence Analysis
  • Pancreas / pathology
  • Polymerase Chain Reaction
  • Receptors, Notch / metabolism*
  • Signal Transduction / immunology
  • Signal Transduction / physiology*
  • T-Lymphocyte Subsets / immunology
  • Thymus Gland / cytology
  • Thymus Gland / immunology
  • fms-Like Tyrosine Kinase 3 / genetics
  • fms-Like Tyrosine Kinase 3 / metabolism

Substances

  • Adaptor Proteins, Signal Transducing
  • Antibodies
  • Calcium-Binding Proteins
  • DLL4 protein, mouse
  • DNA Primers
  • Intracellular Signaling Peptides and Proteins
  • Membrane Glycoproteins
  • Membrane Proteins
  • Receptors, Notch
  • nicastrin protein
  • Flt3 protein, mouse
  • fms-Like Tyrosine Kinase 3
  • Amyloid Precursor Protein Secretases