PMID- 29273394
OWN - NLM
STAT- MEDLINE
DCOM- 20191028
LR  - 20211109
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Print)
IS  - 0161-5890 (Linking)
VI  - 110
DP  - 2019 Jun
TI  - STING, DCs and the link between innate and adaptive tumor immunity.
PG  - 13-23
LID - S0161-5890(17)30594-1 [pii]
LID - 10.1016/j.molimm.2017.12.001 [doi]
AB  - Cancer and the immune system are intimately related. Much of the bulk of tumors 
      is comprised of stromal leukocytes with immune functions, which serve to both 
      promote and inhibit tumor growth, invasion and metastasis. The T lymphocytes of 
      the adaptive immune system are essential for tumor immunity, and these T cells 
      are generated by cross-priming against tumor associated antigens. Dendritic cells 
      (DCs) are essential in this process, serving as the cellular link between innate 
      and adaptive immunity. As a prerequisite for priming of adaptive immune 
      responses, DCs must take up tumor antigens, process them and present them in the 
      context of the major histocompatibility complex (MHC). DCs also serve as sensors 
      of innate activation signals from cancer that are necessary for their activation 
      and effective priming of cancer specific T cells. Here we discuss the role of DCs 
      in the sensing of cancer and in priming the adaptive response against tumors. 
      Furthermore, we present the essential role of the Stimulator of Interferon Genes 
      (STING) signaling pathway in producing type I interferons (IFNs) that are 
      essential in this process.
CI  - Copyright (c) 2017 The Authors. Published by Elsevier Ltd.. All rights reserved.
FAU - Vatner, Ralph E
AU  - Vatner RE
AD  - Division of Immunobiology, Cincinnati Children's Hospital Medical Center, 3333 
      Burnet Avenue, MLC 7038, Cincinnati, OH 45229, United States; Department of 
      Radiation Oncology, University of Cincinnati College of Medicine, 234 Goodman 
      Street, ML 0757, Cincinnati, OH 45267, United States. Electronic address: 
      Ralph.Vatner@UC.edu.
FAU - Janssen, Edith M
AU  - Janssen EM
AD  - Division of Immunobiology, Cincinnati Children's Hospital Medical Center, 3333 
      Burnet Avenue, MLC 7038, Cincinnati, OH 45229, United States.
LA  - eng
GR  - R01 AG053498/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20171220
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Antigens, Neoplasm)
RN  - 9008-11-1 (Interferons)
SB  - IM
MH  - Adaptive Immunity/*physiology
MH  - Animals
MH  - Antigens, Neoplasm/genetics/*physiology
MH  - Dendritic Cells/*physiology
MH  - Humans
MH  - Immunity, Innate/*physiology
MH  - Interferons/genetics
MH  - Neoplasms/genetics/*immunology/pathology
MH  - Signal Transduction/physiology
MH  - Tumor Escape/genetics/immunology
PMC - PMC6768428
MID - NIHMS1530636
OTO - NOTNLM
OT  - Cancer immunotherapy
OT  - Dendritic cell
OT  - Interferon
OT  - Radiation therapy
OT  - STING
OT  - Tumor immunity
EDAT- 2017/12/24 06:00
MHDA- 2019/10/29 06:00
PMCR- 2019/09/30
CRDT- 2017/12/24 06:00
PHST- 2017/08/04 00:00 [received]
PHST- 2017/10/30 00:00 [revised]
PHST- 2017/12/01 00:00 [accepted]
PHST- 2017/12/24 06:00 [pubmed]
PHST- 2019/10/29 06:00 [medline]
PHST- 2017/12/24 06:00 [entrez]
PHST- 2019/09/30 00:00 [pmc-release]
AID - S0161-5890(17)30594-1 [pii]
AID - 10.1016/j.molimm.2017.12.001 [doi]
PST - ppublish
SO  - Mol Immunol. 2019 Jun;110:13-23. doi: 10.1016/j.molimm.2017.12.001. Epub 2017 Dec 
      20.