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

Immunity | Aug 28, 2002

http://www.ncbi.nlm.nih.gov/pubmed/12196292

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 RIS Download

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

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Associated grants

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

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