PMID- 29749614
OWN - NLM
STAT- MEDLINE
DCOM- 20190108
LR  - 20240330
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Print)
IS  - 0019-2805 (Linking)
VI  - 155
IP  - 1
DP  - 2018 Sep
TI  - MicroRNA signature of central nervous system-infiltrating dendritic cells in an 
      animal model of multiple sclerosis.
PG  - 112-122
LID - 10.1111/imm.12934 [doi]
AB  - Innate immune cells are integral to the pathogenesis of several diseases of the 
      central nervous system (CNS), including multiple sclerosis (MS). Dendritic cells 
      (DCs) are potent CD11c(+) antigen-presenting cells that are critical regulators 
      of adaptive immune responses, particularly in autoimmune diseases such as MS. The 
      regulation of DC function in both the periphery and CNS compartment has not been 
      fully elucidated. One limitation to studying the role of CD11c(+) DCs in the CNS 
      is that microglia can upregulate CD11c during inflammation, making it challenging 
      to distinguish bone marrow-derived DCs (BMDCs) from microglia. Selective 
      expression of microRNAs (miRNAs) has been shown to distinguish populations of 
      innate cells and regulate their function within the CNS during 
      neuro-inflammation. Using the experimental autoimmune encephalomyelitis (EAE) 
      murine model of MS, we characterized the expression of miRNAs in CD11c(+) cells 
      using a non-biased murine array. Several miRNAs, including miR-31, were enriched 
      in CD11c(+) cells within the CNS during EAE, but not LysM(+) microglia. Moreover, 
      to distinguish CD11c(+) DCs from microglia that upregulate CD11c, we generated 
      bone marrow chimeras and found that miR-31 expression was specific to BMDCs. 
      Interestingly, miR-31-binding sites were enriched in mRNAs downregulated in BMDCs 
      that migrated into the CNS, and a subset was confirmed to be regulated by miR-31. 
      Finally, miR-31 was elevated in DCs migrating through an in vitro blood-brain 
      barrier. Our findings suggest miRNAs, including miR-31, may regulate entry of DCs 
      into the CNS during EAE, and could potentially represent therapeutic targets for 
      CNS autoimmune diseases such as MS.
CI  - (c) 2018 John Wiley & Sons Ltd.
FAU - Hoye, Mariah L
AU  - Hoye ML
AD  - Department of Neurology, Washington University School of Medicine, St Louis, MO, 
      USA.
FAU - Archambault, Angela S
AU  - Archambault AS
AD  - Department of Neurology, Washington University School of Medicine, St Louis, MO, 
      USA.
FAU - Gordon, Taylor M
AU  - Gordon TM
AD  - Department of Neurology, Washington University School of Medicine, St Louis, MO, 
      USA.
FAU - Oetjen, Landon K
AU  - Oetjen LK
AD  - Department of Medicine, Washington University School of Medicine, St Louis, MO, 
      USA.
FAU - Cain, Matthew D
AU  - Cain MD
AD  - Department of Medicine, Washington University School of Medicine, St Louis, MO, 
      USA.
FAU - Klein, Robyn S
AU  - Klein RS
AD  - Department of Medicine, Washington University School of Medicine, St Louis, MO, 
      USA.
AD  - The Hope Center for Neurological Disorders, Washington University School of 
      Medicine, St Louis, MO, USA.
FAU - Crosby, Seth D
AU  - Crosby SD
AD  - Genome Technology Access Center, Washington University School of Medicine, St 
      Louis, MO, USA.
FAU - Kim, Brian S
AU  - Kim BS
AD  - Department of Medicine, Washington University School of Medicine, St Louis, MO, 
      USA.
AD  - Department of Immunology & Pathology, Washington University School of Medicine, 
      St Louis, MO, USA.
AD  - Center for the Study of Itch, Washington University School of Medicine, St Louis, 
      MO, USA.
FAU - Miller, Timothy M
AU  - Miller TM
AD  - Department of Neurology, Washington University School of Medicine, St Louis, MO, 
      USA.
AD  - The Hope Center for Neurological Disorders, Washington University School of 
      Medicine, St Louis, MO, USA.
FAU - Wu, Gregory F
AU  - Wu GF
AUID- ORCID: 0000-0003-3588-0637
AD  - Department of Neurology, Washington University School of Medicine, St Louis, MO, 
      USA.
AD  - The Hope Center for Neurological Disorders, Washington University School of 
      Medicine, St Louis, MO, USA.
AD  - Department of Immunology & Pathology, Washington University School of Medicine, 
      St Louis, MO, USA.
LA  - eng
GR  - R01 NS083678/NS/NINDS NIH HHS/United States
GR  - F31 NS092340/NS/NINDS NIH HHS/United States
GR  - F31NS092340/NS/NINDS NIH HHS/United States
GR  - R01NS083678/NS/NINDS NIH HHS/United States
GR  - R01NS078398/NS/NINDS NIH HHS/United States
GR  - R01 NS078398/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20180510
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - Central Nervous System/*immunology
MH  - Dendritic Cells/cytology/*immunology/*metabolism
MH  - Disease Models, Animal
MH  - Encephalomyelitis, Autoimmune, Experimental/*immunology
MH  - Inflammation/immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - MicroRNAs/*immunology
MH  - Multiple Sclerosis/*immunology
PMC - PMC6099169
OTO - NOTNLM
OT  - dendritic cells
OT  - microRNAs
OT  - multiple sclerosis
OT  - neuroinflammation
EDAT- 2018/05/12 06:00
MHDA- 2019/01/09 06:00
PMCR- 2019/09/01
CRDT- 2018/05/12 06:00
PHST- 2017/10/05 00:00 [received]
PHST- 2018/02/28 00:00 [revised]
PHST- 2018/03/23 00:00 [accepted]
PHST- 2018/05/12 06:00 [pubmed]
PHST- 2019/01/09 06:00 [medline]
PHST- 2018/05/12 06:00 [entrez]
PHST- 2019/09/01 00:00 [pmc-release]
AID - IMM12934 [pii]
AID - 10.1111/imm.12934 [doi]
PST - ppublish
SO  - Immunology. 2018 Sep;155(1):112-122. doi: 10.1111/imm.12934. Epub 2018 May 10.