PMID- 31753553
OWN - NLM
STAT- MEDLINE
DCOM- 20210107
LR  - 20210107
IS  - 1878-3279 (Electronic)
IS  - 0171-2985 (Linking)
VI  - 225
IP  - 1
DP  - 2020 Jan
TI  - Effect of laminin environments and tumor factors on the biology of myeloid 
      dendritic cells.
PG  - 151854
LID - S0171-2985(19)30176-7 [pii]
LID - 10.1016/j.imbio.2019.10.003 [doi]
AB  - Dendritic cells (DCs) are immune cells that surveil the organism for infections 
      or malignancies and activate specific T lymphocytes initiating specific immune 
      responses. Contrariwise, DCs have been show to participate in the development of 
      diseases, among them some types of cancer by inducing angiogenesis or 
      immunosuppression. The ultimate fate of DC functions regarding their role in 
      disease or health is prompted by signals from the microenvironment. We have 
      previously shown that the interaction of DCs with various extracellular matrix 
      components modifies the immune properties and angiogenic potential of these 
      cells. The objective of the current studies was to investigate the angiogenic and 
      immune profile of murine myeloid DCs upon interaction with laminin environments, 
      with a particular emphasis on ovarian cancer. Our results show that murine 
      ovarian tumors produce several types of laminins, as determined by PCR analysis, 
      and also that tumor-associated DCs, both from ascites or solid tumors express 
      adhesion molecules capable of interacting with these molecules as determined by 
      flow cytometry and PCR analysis. Further, we established that DCs cultured on 
      laminin upregulate both AKT and MEK signaling pathways, and that long-term 
      culture on laminin surfaces decreases the immunological capacities of these cells 
      when compared to the same cells cultured on synthetic substrates. In addition, we 
      observed that tumor conditioned media was able to modify the metabolic status of 
      these cells, and also reprogram the development of DCs from bone marrow 
      precursors towards the generation of myeloid-derived suppressor cells. Overall, 
      these studies demonstrate that the interaction between soluble factors and 
      extracellular matrix components of the ovarian cancer microenvironment shape the 
      biology of DCs and thus help them become co-conspirators of tumor growth.
CI  - Copyright (c) 2019 Elsevier GmbH. All rights reserved.
FAU - Phillippi, Ben
AU  - Phillippi B
AD  - Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio 
      University, United States.
FAU - Singh, Manindra
AU  - Singh M
AD  - Molecular and Cellular Biology Program, Ohio University, United States.
FAU - Loftus, Tiffany
AU  - Loftus T
AD  - Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio 
      University, United States.
FAU - Smith, Hannah
AU  - Smith H
AD  - Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio 
      University, United States.
FAU - Muccioli, Maria
AU  - Muccioli M
AD  - Molecular and Cellular Biology Program, Ohio University, United States.
FAU - Wright, Julia
AU  - Wright J
AD  - Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio 
      University, United States.
FAU - Pate, Michelle
AU  - Pate M
AD  - Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio 
      University, United States.
FAU - Benencia, Fabian
AU  - Benencia F
AD  - Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio 
      University, United States; Molecular and Cellular Biology Program, Ohio 
      University, United States; Biomedical Engineering Program, Russ College of 
      Engineering and Technology, Ohio University, United States; The Diabetes 
      Institute at Ohio University, United States. Electronic address: 
      benencia@ohio.edu.
LA  - eng
GR  - R15 CA137499/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20191110
PL  - Netherlands
TA  - Immunobiology
JT  - Immunobiology
JID - 8002742
RN  - 0 (Antigens, Neoplasm)
RN  - 0 (Laminin)
SB  - IM
MH  - Animals
MH  - Antigens, Neoplasm/immunology
MH  - Carcinogenesis
MH  - Cell Line, Tumor
MH  - Dendritic Cells/*physiology
MH  - Disease Models, Animal
MH  - Extracellular Matrix/*metabolism
MH  - Female
MH  - Humans
MH  - Laminin/genetics/*metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Myeloid Cells/*physiology
MH  - Neovascularization, Pathologic
MH  - Ovarian Neoplasms/*immunology
MH  - Tumor Microenvironment
OTO - NOTNLM
OT  - Bone marrow precursors
OT  - Dendritic cells
OT  - Laminin
OT  - Myeloid-derived suppressor cells
OT  - Ovarian cancer
COIS- Declaration of Competing Interest The authors declare no conflict of interest.
EDAT- 2019/11/23 06:00
MHDA- 2021/01/08 06:00
CRDT- 2019/11/23 06:00
PHST- 2019/05/28 00:00 [received]
PHST- 2019/09/26 00:00 [revised]
PHST- 2019/10/01 00:00 [accepted]
PHST- 2019/11/23 06:00 [pubmed]
PHST- 2021/01/08 06:00 [medline]
PHST- 2019/11/23 06:00 [entrez]
AID - S0171-2985(19)30176-7 [pii]
AID - 10.1016/j.imbio.2019.10.003 [doi]
PST - ppublish
SO  - Immunobiology. 2020 Jan;225(1):151854. doi: 10.1016/j.imbio.2019.10.003. Epub 
      2019 Nov 10.