PMID- 21832159
OWN - NLM
STAT- MEDLINE
DCOM- 20111109
LR  - 20211020
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 187
IP  - 6
DP  - 2011 Sep 15
TI  - TRAIL/DR5 plays a critical role in NK cell-mediated negative regulation of 
      dendritic cell cross-priming of T cells.
PG  - 3087-95
LID - 10.4049/jimmunol.1003879 [doi]
AB  - Dendritic cells (DCs) are critical in initiating immune responses by 
      cross-priming of tumor Ags to T cells. Previous results showed that NK cells 
      inhibited DC-mediated cross-presentation of tumor Ags both in vivo and in vitro. 
      In this study, enhanced Ag presentation was observed in draining lymph nodes in 
      TRAIL(-/-) and DR5(-/-) mice compared with that of wild-type mice. NK cells 
      inhibit DC cross-priming of tumor Ags in vitro, but not direct presentation of 
      endogenous Ags. NK cells lacking TRAIL, but not perforin, were not able to 
      inhibit DC cross-priming of tumor Ags. DCs that lack expression of TRAIL receptor 
      DR5 were less susceptible to NK cell-mediated inhibition of cross-priming, and 
      cross-linking of DR5 receptor led to reduced generation of MHC class I-Ag peptide 
      complexes, followed by attenuated cross-priming of CD8(+) T cells. In addition, 
      key molecules involved in the TRAIL/DR5 pathway during DC/NK cell interactions 
      were determined. In summary, these data indicate a novel alternative pathway for 
      DC/NK cell interactions in antitumor immunity and may reflect homeostasis of both 
      DCs and NK cells for regulation of CD8(+) T cell function in physiological 
      conditions.
FAU - Iyori, Mitsuhiro
AU  - Iyori M
AD  - Department of Microbiology and Immunology, Dartmouth Medical School, Lebanon, NH 
      03756, USA.
FAU - Zhang, Tong
AU  - Zhang T
FAU - Pantel, Haddon
AU  - Pantel H
FAU - Gagne, Bethany A
AU  - Gagne BA
FAU - Sentman, Charles L
AU  - Sentman CL
LA  - eng
GR  - CA101748/CA/NCI NIH HHS/United States
GR  - R01 CA101748-05/CA/NCI NIH HHS/United States
GR  - P30 CA023108/CA/NCI NIH HHS/United States
GR  - R01 CA130911/CA/NCI NIH HHS/United States
GR  - R01 CA101748/CA/NCI NIH HHS/United States
GR  - CA130911/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20110810
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (Tnfsf10 protein, mouse)
SB  - IM
MH  - Animals
MH  - Antigen Presentation/immunology
MH  - Cell Separation
MH  - Cross-Priming/*immunology
MH  - Dendritic Cells/*immunology/metabolism
MH  - Flow Cytometry
MH  - Killer Cells, Natural/*immunology/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Receptors, TNF-Related Apoptosis-Inducing Ligand/*immunology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - T-Lymphocytes/*immunology/metabolism
MH  - TNF-Related Apoptosis-Inducing Ligand/*immunology
PMC - PMC3169733
MID - NIHMS312001
COIS- Conflict of interest The authors declare no financial or commercial conflict of 
      interest.
EDAT- 2011/08/13 06:00
MHDA- 2011/11/10 06:00
PMCR- 2012/09/15
CRDT- 2011/08/12 06:00
PHST- 2011/08/12 06:00 [entrez]
PHST- 2011/08/13 06:00 [pubmed]
PHST- 2011/11/10 06:00 [medline]
PHST- 2012/09/15 00:00 [pmc-release]
AID - jimmunol.1003879 [pii]
AID - 10.4049/jimmunol.1003879 [doi]
PST - ppublish
SO  - J Immunol. 2011 Sep 15;187(6):3087-95. doi: 10.4049/jimmunol.1003879. Epub 2011 
      Aug 10.