PMID- 23280948
OWN - NLM
STAT- MEDLINE
DCOM- 20130823
LR  - 20130305
IS  - 1099-1654 (Electronic)
IS  - 1052-9276 (Linking)
VI  - 23
IP  - 2
DP  - 2013 Mar
TI  - Contribution of dendritic cells to measles virus induced immunosuppression.
PG  - 126-38
LID - 10.1002/rmv.1735 [doi]
AB  - Measles virus (MV) remains an important pathogen in children worldwide. The 
      morbidity and mortality of MV is associated with severe immune suppression. 
      Dendritic cells (DCs) were identified as initial target cells in vivo, and DCs 
      were efficiently infected by MV in vitro. MV infection of DCs likely contributes 
      to functional deficiency in these cells; therefore playing a role in MV-induced 
      immunosuppression. DCs appeared to mature phenotypically; however, the ability of 
      infected cells to stimulate T cells was compromised. Phenotypic maturation of 
      infected immature DCs was partially controlled by IFN production; however, 
      infected DCs also maintained markers of an immature phenotype such as the 
      continued uptake of antigen and lack of expression of chemokine receptor CCR7. 
      Furthermore, mature DCs did not appear to maintain phenotypic maturation 
      following infection demonstrated by decreased MHC and co-stimulatory molecule 
      expression. Several mechanisms of MV-induced DC dysfunction have been suggested, 
      each likely contributing to the immunosuppressive effect of MV-infected DCs. 
      Infected DCs responded aberrantly to secondary maturation stimuli such as CD40L 
      or TLR4 stimulation. MV infection resulted in apoptosis in DC/T-cell cocultures, 
      which may contribute to a reduced T-cell response. Additionally, the 
      immunological synapse between infected DCs and T cells was compromised resulting 
      in reduced T-cell interaction times and activation signaling. The mechanisms of 
      MV contribution to DC dysfunction appear multifaceted and central to MV-induced 
      immunosuppression.
CI  - Published 2012. This article is a U.S. Government work and is in the public 
      domain in the USA.
FAU - Coughlin, Melissa M
AU  - Coughlin MM
AD  - Centers for Disease Control and Prevention, Measles, Mumps, Rubella and 
      Herpesvirus Laboratory Branch, Atlanta, GA 30333, USA.
FAU - Bellini, William J
AU  - Bellini WJ
FAU - Rota, Paul A
AU  - Rota PA
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
DEP - 20121220
PL  - England
TA  - Rev Med Virol
JT  - Reviews in medical virology
JID - 9112448
SB  - IM
MH  - Apoptosis
MH  - Dendritic Cells/*immunology
MH  - Humans
MH  - *Immune Evasion
MH  - Immune Tolerance
MH  - Measles virus/*immunology/pathogenicity
MH  - T-Lymphocytes/immunology
EDAT- 2013/01/03 06:00
MHDA- 2013/08/24 06:00
CRDT- 2013/01/03 06:00
PHST- 2012/06/25 00:00 [received]
PHST- 2012/10/29 00:00 [revised]
PHST- 2012/10/30 00:00 [accepted]
PHST- 2013/01/03 06:00 [entrez]
PHST- 2013/01/03 06:00 [pubmed]
PHST- 2013/08/24 06:00 [medline]
AID - 10.1002/rmv.1735 [doi]
PST - ppublish
SO  - Rev Med Virol. 2013 Mar;23(2):126-38. doi: 10.1002/rmv.1735. Epub 2012 Dec 20.