PMID- 12462394
OWN - NLM
STAT- MEDLINE
DCOM- 20030528
LR  - 20190922
IS  - 1566-5240 (Print)
IS  - 1566-5240 (Linking)
VI  - 2
IP  - 8
DP  - 2002 Dec
TI  - Dendritic cells in innate immune responses against HIV.
PG  - 739-56
AB  - Dendritic cells (DCs) were recently found to be innate immunity effectors against 
      tumoral cells and viruses. (i) In response to most viruses, including HIV, 
      plasmacytoid DCs are responsible for most of the type I IFN secretion, which is 
      strongly anti-viral and induces TH1 type responses. Myeloid DCs secrete IL-12, 
      which is also important for TH1-type and cytotoxic responses. In HIV patient 
      blood, both DC population numbers decrease as early as the primary stage. 
      Plasmacytoid DC numbers correlate with type I IFN secretion, which is a prognosis 
      predictor, particularly under treatment. IL-12 secretion is also defective. 
      Immunotherapies to replace the defective cytokines or to restore a potentially 
      defective DC-T lymphocyte feed-back might help patients restore their immune 
      responses under antiviral therapy. (ii) After measles and other viral infections, 
      or incubation with dsRNA, DCs become cytotoxic and consequently exhibit natural 
      killer function, through upregulation of type I IFN secretion which enhances 
      TRAIL expression. In HIV infection, this mechanism was not demonstrated yet, but 
      it might a) be responsible for the massive apoptosis of uninfected lymphocytes, 
      and b) increase specific immunity through cross-presentation of antigens from 
      infected cells killed by DCs. (iii) DCs direct expansion and effector functions 
      of NK cells in the absence of adaptive-type cytokines and modulate NKT cell 
      IFN-gamma production. Reciprocally, NK activation triggers DC maturation. HIV-1 
      Tat inhibits NK cell cytotoxicity directly and probably through inhibition of 
      IL-12 secretion by DC. Therefore, understanding the functions of DCs in innate 
      immune responses and in pathogenesis will help obtain better HIV replication 
      control.
FAU - Servet, C
AU  - Servet C
AD  - Immunobiologie Fondamentale et Clinique, CERVI-INSERM U503, 21 avenue Tony 
      Garnier, 69007 Lyon, France.
FAU - Zitvogel, L
AU  - Zitvogel L
FAU - Hosmalin, A
AU  - Hosmalin A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Netherlands
TA  - Curr Mol Med
JT  - Current molecular medicine
JID - 101093076
RN  - 0 (Antigens, CD34)
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (CD40 Antigens)
RN  - 0 (Ligands)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (TNFSF10 protein, human)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Acquired Immunodeficiency Syndrome/therapy
MH  - Animals
MH  - Antigen Presentation
MH  - Antigens, CD34/biosynthesis
MH  - Apoptosis Regulatory Proteins
MH  - CD40 Antigens/biosynthesis
MH  - Cell Differentiation
MH  - Dendritic Cells/*immunology/*virology
MH  - HIV/*metabolism
MH  - HIV Infections
MH  - Humans
MH  - Interleukin-12/metabolism
MH  - Killer Cells, Natural/immunology/metabolism
MH  - Ligands
MH  - Membrane Glycoproteins/biosynthesis
MH  - Models, Biological
MH  - Neuroblastoma/therapy
MH  - T-Lymphocytes/metabolism
MH  - TNF-Related Apoptosis-Inducing Ligand
MH  - Th1 Cells/metabolism
MH  - Tumor Necrosis Factor-alpha/biosynthesis
RF  - 205
EDAT- 2002/12/05 04:00
MHDA- 2003/05/29 05:00
CRDT- 2002/12/05 04:00
PHST- 2002/12/05 04:00 [pubmed]
PHST- 2003/05/29 05:00 [medline]
PHST- 2002/12/05 04:00 [entrez]
AID - 10.2174/1566524023361907 [doi]
PST - ppublish
SO  - Curr Mol Med. 2002 Dec;2(8):739-56. doi: 10.2174/1566524023361907.