PMID- 22075702
OWN - NLM
STAT- MEDLINE
DCOM- 20120207
LR  - 20231213
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 187
IP  - 12
DP  - 2011 Dec 15
TI  - Th-1 lymphocytes induce dendritic cell tumor killing activity by an 
      IFN-gamma-dependent mechanism.
PG  - 6310-7
LID - 10.4049/jimmunol.1101812 [doi]
AB  - Dendritic cells (DCs) encompass a heterogeneous population of cells capable of 
      orchestrating innate and adaptive immune responses. The ability of DCs to act as 
      professional APCs has been the foundation for the development and use of these 
      cells as vaccines in cancer immunotherapy. DCs are also endowed with the 
      nonconventional property of directly killing tumor cells. The current study 
      investigates the regulation of murine DC cytotoxic function by T lymphocytes. We 
      provide evidence that CD4(+) Th-1, but not Th-2, Th-17 cells, or regulatory T 
      cells, are capable of inducing DC cytotoxic function. IFN-gamma was identified as the 
      major factor responsible for Th-1-induced DC tumoricidal activity. Tumor cell 
      killing mediated by Th-1-activated killer DCs was dependent on inducible NO 
      synthase expression and NO production. Importantly, Th-1-activated killer DCs 
      were capable of presenting the acquired Ags from the killed tumor cells to T 
      lymphocytes in vitro or in vivo. These observations offer new possibilities for 
      the application of killer DCs in cancer immunotherapy.
FAU - LaCasse, Collin J
AU  - LaCasse CJ
AD  - Department of Pediatrics, University of Arizona, Tucson, AZ 85724-5073, USA.
FAU - Janikashvili, Nona
AU  - Janikashvili N
FAU - Larmonier, Claire B
AU  - Larmonier CB
FAU - Alizadeh, Darya
AU  - Alizadeh D
FAU - Hanke, Neale
AU  - Hanke N
FAU - Kartchner, Jessica
AU  - Kartchner J
FAU - Situ, Elaine
AU  - Situ E
FAU - Centuori, Sara
AU  - Centuori S
FAU - Har-Noy, Michael
AU  - Har-Noy M
FAU - Bonnotte, Bernard
AU  - Bonnotte B
FAU - Katsanis, Emmanuel
AU  - Katsanis E
FAU - Larmonier, Nicolas
AU  - Larmonier N
LA  - eng
GR  - P30 CA023074/CA/NCI NIH HHS/United States
GR  - CA023074/CA/NCI NIH HHS/United States
GR  - R01 CA104926/CA/NCI NIH HHS/United States
GR  - T32CA009213/CA/NCI NIH HHS/United States
GR  - T32 CA009213-34/CA/NCI NIH HHS/United States
GR  - T32 CA009213/CA/NCI NIH HHS/United States
GR  - R01 CA104926-06/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 - 20111109
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Receptors, Interferon)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Antigen Presentation/genetics/immunology
MH  - Bone Marrow Cells/cytology/immunology/metabolism
MH  - Cell Line, Tumor
MH  - Coculture Techniques
MH  - *Cytotoxicity, Immunologic/genetics
MH  - Dendritic Cells/*immunology/metabolism
MH  - Female
MH  - Interferon-gamma/metabolism/*physiology
MH  - Mammary Neoplasms, Experimental/*immunology/pathology/therapy
MH  - Melanoma, Experimental/*immunology/pathology/therapy
MH  - Mice
MH  - Mice, 129 Strain
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Receptors, Interferon/deficiency/genetics/*physiology
MH  - Th1 Cells/*immunology/*metabolism
MH  - Interferon gamma Receptor
PMC - PMC3297475
MID - NIHMS332197
EDAT- 2011/11/15 06:00
MHDA- 2012/02/09 06:00
PMCR- 2012/12/15
CRDT- 2011/11/15 06:00
PHST- 2011/11/15 06:00 [entrez]
PHST- 2011/11/15 06:00 [pubmed]
PHST- 2012/02/09 06:00 [medline]
PHST- 2012/12/15 00:00 [pmc-release]
AID - jimmunol.1101812 [pii]
AID - 10.4049/jimmunol.1101812 [doi]
PST - ppublish
SO  - J Immunol. 2011 Dec 15;187(12):6310-7. doi: 10.4049/jimmunol.1101812. Epub 2011 
      Nov 9.