PMID- 24759079
OWN - NLM
STAT- MEDLINE
DCOM- 20140730
LR  - 20220330
IS  - 1090-2163 (Electronic)
IS  - 0008-8749 (Print)
IS  - 0008-8749 (Linking)
VI  - 289
IP  - 1-2
DP  - 2014 May-Jun
TI  - Dendritic-cell exosomes cross-present Toll-like receptor-ligands and activate 
      bystander dendritic cells.
PG  - 119-27
LID - S0008-8749(14)00061-6 [pii]
LID - 10.1016/j.cellimm.2014.03.016 [doi]
AB  - Dendritic cells (DCs) are the major sentinel, antigen-presenting and regulatory 
      components of the immune system. One of the central DC functions is to rapidly 
      sense and alert host immune system of a pathogen invasion. In the present study, 
      we investigated the role of DC exosomes (DCex) in this sentinel function. We 
      demonstrated that DCex could bind bacterial Toll-like-receptor ligands (TLR-Ls), 
      and acquire their ability to strongly activate bystander DCs. Consequently, 
      bystander DCs enhance the expression of transmembrane tumor necrosis factor, 
      secretion of proinflammatory cytokines and cross-talk with natural killer cells 
      leading to the elevated secretion of IFNgamma. These findings newly show that DCex 
      can bind and cross-present TLR-Ls to innate-immunity effector cells, and indicate 
      a potent mechanism to systemically alert the host immune system of pathogen 
      invasion. They also suggest a potential novel strategy to generate effective 
      vaccines by binding TLR-L-immune adjuvants to DCex.
CI  - Published by Elsevier Inc.
FAU - Sobo-Vujanovic, Andrea
AU  - Sobo-Vujanovic A
AD  - University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA.
FAU - Munich, Stephan
AU  - Munich S
AD  - Rush University Medical Center, Department of Neurosurgery, Chicago, IL, USA.
FAU - Vujanovic, Nikola L
AU  - Vujanovic NL
AD  - University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA; Department of 
      Pathology, Pittsburgh, PA, USA; Department of Immunology, Pittsburgh, PA, USA. 
      Electronic address: vujanovicnl@msx.upmc.edu.
LA  - eng
GR  - R01 DE17150/DE/NIDCR NIH HHS/United States
GR  - P30 CA047904/CA/NCI NIH HHS/United States
GR  - R01 DE014775/DE/NIDCR NIH HHS/United States
GR  - P30CA047904/CA/NCI NIH HHS/United States
GR  - P60 DE013059/DE/NIDCR NIH HHS/United States
GR  - DE13059/DE/NIDCR NIH HHS/United States
GR  - R01 DE017150/DE/NIDCR NIH HHS/United States
GR  - R01 DE14775/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20140408
PL  - Netherlands
TA  - Cell Immunol
JT  - Cellular immunology
JID - 1246405
RN  - 0 (Bacterial Outer Membrane Proteins)
RN  - 0 (Lipopeptides)
RN  - 0 (Pam(3)CSK(4) peptide)
RN  - 0 (TLR protein, bacteria)
RN  - 0 (Toll-Like Receptor 1)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Antigen Presentation/immunology
MH  - Bacterial Outer Membrane Proteins/*immunology
MH  - Bystander Effect/*immunology
MH  - Dendritic Cells/*immunology
MH  - Exosomes/*immunology
MH  - Female
MH  - Interferon-gamma/metabolism
MH  - Killer Cells, Natural/*immunology
MH  - Lipopeptides/immunology
MH  - Lymphocyte Activation/immunology
MH  - Mice
MH  - Mice, Knockout
MH  - Mice, SCID
MH  - Toll-Like Receptor 1/agonists
MH  - Toll-Like Receptor 2/agonists
MH  - Tumor Necrosis Factor-alpha/immunology
PMC - PMC4045011
MID - NIHMS584447
OTO - NOTNLM
OT  - Dendritic cells
OT  - Exosomes
OT  - NK cells
OT  - TLR ligands
OT  - Th1 response
OT  - Transmembrane TNF
EDAT- 2014/04/25 06:00
MHDA- 2014/07/31 06:00
PMCR- 2015/05/01
CRDT- 2014/04/25 06:00
PHST- 2013/10/14 00:00 [received]
PHST- 2013/12/23 00:00 [revised]
PHST- 2014/03/31 00:00 [accepted]
PHST- 2014/04/25 06:00 [entrez]
PHST- 2014/04/25 06:00 [pubmed]
PHST- 2014/07/31 06:00 [medline]
PHST- 2015/05/01 00:00 [pmc-release]
AID - S0008-8749(14)00061-6 [pii]
AID - 10.1016/j.cellimm.2014.03.016 [doi]
PST - ppublish
SO  - Cell Immunol. 2014 May-Jun;289(1-2):119-27. doi: 10.1016/j.cellimm.2014.03.016. 
      Epub 2014 Apr 8.