PMID- 18614931
OWN - NLM
STAT- MEDLINE
DCOM- 20080903
LR  - 20231213
IS  - 1525-4135 (Print)
IS  - 1525-4135 (Linking)
VI  - 48
IP  - 4
DP  - 2008 Aug 1
TI  - Candida albicans-induced DC activation partially restricts HIV amplification in 
      DCs and increases DC to T-cell spread of HIV.
PG  - 398-407
LID - 10.1097/QAI.0b013e3181776bc7 [doi]
AB  - Dendritic cells (DCs) are central to the innate and adaptive responses needed to 
      control pathogens, yet HIV exploits DCs to promote infection. The influence of 
      other pathogens on DC-HIV interplay has not been extensively studied. We used 
      Candida albicans (Candida) as a model pathogen which elicits innate DC responses 
      that are likely important in controlling Candida by healthy immune systems. HIV 
      did not impede Candida-specific DC activation. Candida-induced CD80 and CD83 
      upregulation was greater in DCs that had captured HIV, coinciding with increased 
      amplification in presence of T cells and reduced but persistent low-level DC 
      infection. In contrast, HIV-infected DCs matured normally in response to Candida, 
      but this did not shut down HIV replication in DCs, and again Candida augmented 
      HIV amplification in DC-T-cell mixtures. HIV-infected DCs secreted more IL-10 and 
      IL-1beta earlier than uninfected DCs and initially induced a higher frequency of 
      CD4CD25FoxP3 T-regulatory cells in response to Candida. Elevated early IL-10 
      production in cocultures was evident only when azidothymidine (AZT) was included 
      to limit T-regulatory cell infection and destruction. Therefore, HIV manipulates 
      the DC's innate and adaptive responses to Candida to further augment HIV spread, 
      ultimately destroying the cells needed to limit candidiasis.
FAU - Vachot, Laurence
AU  - Vachot L
AD  - Center for Biomedical Research, Population Council, 1230 York Avenue, New York, 
      NY 10065, USA.
FAU - Williams, Vennansha G
AU  - Williams VG
FAU - Bess, Julian W Jr
AU  - Bess JW Jr
FAU - Lifson, Jeffrey D
AU  - Lifson JD
FAU - Robbiani, Melissa
AU  - Robbiani M
LA  - eng
GR  - A1040877/PHS HHS/United States
GR  - AI065412/AI/NIAID NIH HHS/United States
GR  - AI065413/AI/NIAID NIH HHS/United States
GR  - DE015512/DE/NIDCR NIH HHS/United States
GR  - HD041752/HD/NICHD NIH HHS/United States
GR  - N01-CO-12400/CO/NCI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Acquir Immune Defic Syndr
JT  - Journal of acquired immune deficiency syndromes (1999)
JID - 100892005
RN  - 0 (Antigens, CD)
RN  - 0 (B7-1 Antigen)
RN  - 0 (FOXP3 protein, human)
RN  - 0 (Forkhead Transcription Factors)
RN  - 0 (Immunoglobulins)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Membrane Glycoproteins)
RN  - 130068-27-8 (Interleukin-10)
SB  - IM
MH  - Antigens, CD/metabolism
MH  - B7-1 Antigen/metabolism
MH  - *Candida albicans
MH  - Candidiasis/complications/*immunology
MH  - Cell Count
MH  - Coculture Techniques
MH  - Dendritic Cells/*immunology/metabolism/microbiology
MH  - Forkhead Transcription Factors/biosynthesis
MH  - *HIV
MH  - HIV Infections/complications/*immunology
MH  - Humans
MH  - Immunoglobulins/metabolism
MH  - Interleukin-10/biosynthesis
MH  - Interleukin-1beta/biosynthesis
MH  - Membrane Glycoproteins/metabolism
MH  - T-Lymphocytes, Regulatory/*immunology/virology
MH  - CD83 Antigen
EDAT- 2008/07/11 09:00
MHDA- 2008/09/04 09:00
CRDT- 2008/07/11 09:00
PHST- 2008/07/11 09:00 [pubmed]
PHST- 2008/09/04 09:00 [medline]
PHST- 2008/07/11 09:00 [entrez]
AID - 10.1097/QAI.0b013e3181776bc7 [doi]
PST - ppublish
SO  - J Acquir Immune Defic Syndr. 2008 Aug 1;48(4):398-407. doi: 
      10.1097/QAI.0b013e3181776bc7.