PMID- 23772620
OWN - NLM
STAT- MEDLINE
DCOM- 20140124
LR  - 20211021
IS  - 1600-065X (Electronic)
IS  - 0105-2896 (Print)
IS  - 0105-2896 (Linking)
VI  - 254
IP  - 1
DP  - 2013 Jul
TI  - Dendritic cell dysregulation during HIV-1 infection.
PG  - 170-89
LID - 10.1111/imr.12082 [doi]
AB  - Dendritic cells (DCs) are a diverse subset of innate immune cells that are key 
      regulators of the host response to human immunodeficiency virus-1 (HIV-1) 
      infection. HIV-1 directly and indirectly modulates DC function to hinder the 
      formation of effective antiviral immunity and fuel immune activation. This review 
      focuses upon the differential dysregulation of myeloid DCs (mDCs) and 
      plasmacytoid DCs (pDCs) at various stages of HIV-1 infection providing insights 
      into pathogenesis. HIV-1 evades innate immune sensing by mDCs resulting in 
      suboptimal maturation, lending to poor generation of antiviral adaptive responses 
      and contributing to T-regulatory cell (Treg) development. Dependent upon the 
      stage of HIV-1 infection, mDC function is altered in response to Toll-like 
      receptor ligands, which further hinders adaptive immunity and limits feasibility 
      of therapeutic vaccine strategies. pDC interactions with HIV-1 are pleotropic, 
      modulating immune responses on an axis between immunostimulatory and 
      immunosuppressive. pDCs promote immune activation through an altered phenotype of 
      persistent type I interferon secretion and weak antigen presentation capacity. 
      Conversely, HIV-1 stimulates secretion of indolemine 2,3 dioxygenase (IDO) by 
      pDCs resulting in Treg induction. An improved understanding of the roles and 
      underlying mechanisms of DC dysfunction will be valuable to the development of 
      therapeutics to enhance HIV-specific adaptive responses and to dampen immune 
      activation.
CI  - (c) 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
FAU - Miller, Elizabeth
AU  - Miller E
AD  - Division of Infectious Diseases, New York University School of Medicine, New 
      York, NY, USA.
FAU - Bhardwaj, Nina
AU  - Bhardwaj N
LA  - eng
GR  - R01 AI044628/AI/NIAID NIH HHS/United States
GR  - U01 A1067854/PHS HHS/United States
GR  - AI044628/AI/NIAID NIH HHS/United States
GR  - P01 AI057127/AI/NIAID NIH HHS/United States
GR  - P01AI057127/AI/NIAID NIH HHS/United States
GR  - K08 AI84578/AI/NIAID NIH HHS/United States
GR  - AI081848/AI/NIAID NIH HHS/United States
GR  - R37 AI044628/AI/NIAID NIH HHS/United States
GR  - R01 AI081848/AI/NIAID NIH HHS/United States
GR  - K08 AI084578/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Immunol Rev
JT  - Immunological reviews
JID - 7702118
SB  - IM
MH  - Animals
MH  - Dendritic Cells/*immunology/metabolism/virology
MH  - HIV Infections/*immunology/metabolism
MH  - HIV-1/*immunology
MH  - Humans
MH  - Immunomodulation
PMC - PMC5590719
MID - NIHMS903021
EDAT- 2013/06/19 06:00
MHDA- 2014/01/25 06:00
PMCR- 2017/09/08
CRDT- 2013/06/19 06:00
PHST- 2013/06/19 06:00 [entrez]
PHST- 2013/06/19 06:00 [pubmed]
PHST- 2014/01/25 06:00 [medline]
PHST- 2017/09/08 00:00 [pmc-release]
AID - 10.1111/imr.12082 [doi]
PST - ppublish
SO  - Immunol Rev. 2013 Jul;254(1):170-89. doi: 10.1111/imr.12082.