{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jung S"],"funding":["NEI NIH HHS"],"pagination":["211-20"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3689299"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(2)"],"pubmed_abstract":["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."],"journal":["Immunity"],"pubmed_title":["In vivo depletion of CD11c+ dendritic cells abrogates priming of CD8+ T cells by exogenous cell-associated antigens."],"pmcid":["PMC3689299"],"funding_grant_id":["R01 EY010559-11","R01 EY010559"],"pubmed_authors":["Unutmaz D","Vuthoori S","Wong P","Sparwasser T","Zavala F","Pamer EG","De los Santos K","Ko K","Littman DR","Wu S","Sano G","Lang RA","Jung S"],"additional_accession":[]},"is_claimable":false,"name":"In vivo depletion of CD11c+ dendritic cells abrogates priming of CD8+ T cells by exogenous cell-associated antigens.","description":"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.","dates":{"release":"2002-01-01T00:00:00Z","publication":"2002 Aug","modification":"2021-02-19T20:21:31Z","creation":"2019-03-27T01:11:58Z"},"accession":"S-EPMC3689299","cross_references":{"pubmed":["12196292"],"doi":["10.1016/s1074-7613(02)00365-5"]}}