Characterization of human DNGR-1+ BDCA3+ leukocytes as putative equivalents of mouse CD8alpha+ dendritic cells

J Exp Med. 2010 Jun 7;207(6):1261-71. doi: 10.1084/jem.20092618. Epub 2010 May 17.

Abstract

In mouse, a subset of dendritic cells (DCs) known as CD8alpha+ DCs has emerged as an important player in the regulation of T cell responses and a promising target in vaccination strategies. However, translation into clinical protocols has been hampered by the failure to identify CD8alpha+ DCs in humans. Here, we characterize a population of human DCs that expresses DNGR-1 (CLEC9A) and high levels of BDCA3 and resembles mouse CD8alpha+ DCs in phenotype and function. We describe the presence of such cells in the spleens of humans and humanized mice and report on a protocol to generate them in vitro. Like mouse CD8alpha+ DCs, human DNGR-1+ BDCA3hi DCs express Necl2, CD207, BATF3, IRF8, and TLR3, but not CD11b, IRF4, TLR7, or (unlike CD8alpha+ DCs) TLR9. DNGR-1+ BDCA3hi DCs respond to poly I:C and agonists of TLR8, but not of TLR7, and produce interleukin (IL)-12 when given innate and T cell-derived signals. Notably, DNGR-1+ BDCA3+ DCs from in vitro cultures efficiently internalize material from dead cells and can cross-present exogenous antigens to CD8+ T cells upon treatment with poly I:C. The characterization of human DNGR-1+ BDCA3hi DCs and the ability to grow them in vitro opens the door for exploiting this subset in immunotherapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, Surface / metabolism*
  • CD8-Positive T-Lymphocytes / cytology*
  • CD8-Positive T-Lymphocytes / drug effects
  • CD8-Positive T-Lymphocytes / immunology*
  • Cross-Priming / drug effects
  • Dendritic Cells / cytology*
  • Dendritic Cells / drug effects
  • Dendritic Cells / immunology*
  • Endocytosis / drug effects
  • Endocytosis / immunology
  • Gene Expression Profiling
  • Gene Expression Regulation / drug effects
  • Hematopoietic Stem Cells / cytology
  • Hematopoietic Stem Cells / drug effects
  • Humans
  • Immunity, Innate / drug effects
  • Interleukin-12 / biosynthesis
  • Lectins, C-Type / metabolism*
  • Mice
  • Phenotype
  • Poly I-C / pharmacology
  • Receptors, Mitogen / metabolism*
  • Spleen / cytology
  • Spleen / drug effects
  • Spleen / immunology
  • Thrombomodulin
  • Toll-Like Receptors / agonists

Substances

  • Antigens, Surface
  • CLEC9a protein, human
  • Lectins, C-Type
  • Receptors, Mitogen
  • THBD protein, human
  • Thrombomodulin
  • Toll-Like Receptors
  • Interleukin-12
  • Poly I-C