PMID- 23638101
OWN - NLM
STAT- MEDLINE
DCOM- 20131209
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 4
DP  - 2013
TI  - Differential susceptibility and response of primary human myeloid BDCA1(+) 
      dendritic cells to infection with different Enteroviruses.
PG  - e62502
LID - 10.1371/journal.pone.0062502 [doi]
LID - e62502
AB  - Coxsackie B viruses (CVBs) and echoviruses (EVs) form the Human Enterovirus-B 
      (HEV-B) species within the family Picornaviridae. HEV-B infections are widespread 
      and generally cause mild disease; however, severe infections occur and HEV-B are 
      associated with various chronic diseases such as cardiomyopathy and type 1 
      diabetes. Dendritic cells (DCs) are the professional antigen-presenting cells of 
      our immune system and initiate and control immune responses to invading 
      pathogens, yet also maintain tolerance to self-antigens. We previously reported 
      that EVs, but not CVBs, can productively infect in vitro generated 
      monocyte-derived DCs. The interactions between HEV-B and human myeloid DCs (mDCs) 
      freshly isolated from blood, however, remain unknown. Here, we studied the 
      susceptibility and responses of BDCA1(+) mDC to HEV-B species and found that 
      these mDC are susceptible to EV, but not CVB infection. Productive EV7 infection 
      resulted in massive, rapid cell death without DC activation. Contrary, EV1 
      infection, which resulted in lower virus input at the same MOI, resulted in DC 
      activation as observed by production of type I interferon-stimulated genes 
      (ISGs), upregulation of co-stimulatory and co-inhibitory molecules (CD80, CD86, 
      PDL1) and production of IL-6 and TNF-alpha, with a relative moderate decrease in cell 
      viability. EV1-induced ISG expression depended on virus replication. CVB 
      infection did not affect DC viability and resulted in poor induction of ISGs and 
      CD80 induction in part of the donors. These data show for the first time the 
      interaction between HEV-B species and BDCA1(+) mDCs isolated freshly from blood. 
      Our data indicate that different HEV-B species can influence DC homeostasis in 
      various ways, possibly contributing to HEV-B associated pathology.
FAU - Schulte, Barbara M
AU  - Schulte BM
AD  - Department of Tumor Immunology, Nijmegen Centre for Molecular Life Sciences & 
      Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
FAU - Kers-Rebel, Esther D
AU  - Kers-Rebel ED
FAU - Prosser, Amy C
AU  - Prosser AC
FAU - Galama, Jochem M D
AU  - Galama JM
FAU - van Kuppeveld, Frank J M
AU  - van Kuppeveld FJ
FAU - Adema, Gosse J
AU  - Adema GJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130424
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Antigens, CD1)
RN  - 0 (Antigens, Surface)
RN  - 0 (CD1C protein, human)
RN  - 0 (Glycoproteins)
RN  - 0 (Interferon-alpha)
RN  - 0 (Toll-Like Receptors)
RN  - 77238-31-4 (Interferon-beta)
SB  - IM
MH  - Antigens, CD1
MH  - Antigens, Surface/*metabolism
MH  - Cell Death
MH  - Cell Differentiation/immunology
MH  - Cytopathogenic Effect, Viral
MH  - Dendritic Cells/cytology/immunology/*metabolism/*virology
MH  - Enterovirus/immunology/*physiology
MH  - Glycoproteins
MH  - Humans
MH  - Interferon-alpha/biosynthesis/immunology
MH  - Interferon-beta/biosynthesis/immunology
MH  - Myeloid Cells/immunology/*metabolism/*virology
MH  - Toll-Like Receptors/metabolism
MH  - Virus Replication
PMC - PMC3634769
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/05/03 06:00
MHDA- 2013/12/16 06:00
PMCR- 2013/04/24
CRDT- 2013/05/03 06:00
PHST- 2012/12/14 00:00 [received]
PHST- 2013/03/22 00:00 [accepted]
PHST- 2013/05/03 06:00 [entrez]
PHST- 2013/05/03 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
PHST- 2013/04/24 00:00 [pmc-release]
AID - PONE-D-12-39561 [pii]
AID - 10.1371/journal.pone.0062502 [doi]
PST - epublish
SO  - PLoS One. 2013 Apr 24;8(4):e62502. doi: 10.1371/journal.pone.0062502. Print 2013.