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In vivo depletion of CD11c+ dendritic cells abrogates priming of CD8+ T cells by exogenous cell-associated antigens.

Cytotoxic T lymphocytes (CTL) respond to antigenic peptides presented on MHC class I molecules. On most cells, these peptides are exclusively of endogenous, cytosolic origin. Bone marrow-derived antigen-presenting cells, however, harbor a unique pathway for MHC I presentation of exogenous antigens. This mechanism permits cross-presentation of pathogen-infected cells and the priming of CTL responses against intracellular microbial infections. Here, we report a novel diphtheria toxin-based system that allows the inducible, short-term ablation of dendritic cells (DC) in vivo. We show that in vivo DC are required to cross-prime CTL precursors. Our results thus define a unique in vivo role of DC, i.e., the sensitization of the immune system for cell-associated antigens. DC-depleted mice fail to mount CTL responses to infection with the intracellular bacterium Listeria monocytogenes and the rodent malaria parasite Plasmodium yoelii.

Pubmed ID: 12196292

Authors

  • Jung S
  • Unutmaz D
  • Wong P
  • Sano G
  • De los Santos K
  • Sparwasser T
  • Wu S
  • Vuthoori S
  • Ko K
  • Zavala F
  • Pamer EG
  • Littman DR
  • Lang RA

Journal

Immunity

Publication Data

August 28, 2002

Associated Grants

  • Agency: NEI NIH HHS, Id: R01 EY010559
  • Agency: NEI NIH HHS, Id: R01 EY010559-11

Mesh Terms

  • Animals
  • CD8-Positive T-Lymphocytes
  • Dendritic Cells
  • Diphtheria Toxin
  • Heparin-binding EGF-like Growth Factor
  • Integrin alphaXbeta2
  • Intercellular Signaling Peptides and Proteins
  • Listeria monocytogenes
  • Liver
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Models, Animal
  • Plasmodium yoelii
  • Receptors, Cell Surface
  • Recombinant Fusion Proteins
  • T-Lymphocytes, Cytotoxic