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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
2003-4-8
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pubmed:abstractText |
APC infection and dysfunction may contribute to the immunopathogenesis of HIV disease. In this study, we examined immunologic function of highly enriched populations of HIV-infected monocyte-derived dendritic cells (DC). Compared with uninfected DC, HIV-infected DC markedly down-regulated surface expression of CD4. HIV p24(+) DC were then enriched by negative selection of CD4(+)HIV p24(-) DC and assessed for cytokine secretion and immunologic function. Although enriched populations of HIV-infected DC secreted increased IL-12p70 and decreased IL-10, these cells were poor stimulators of allogeneic CD4(+) T cell proliferation and IL-2 production. Interestingly, HIV-infected DC secreted HIV gp120 and the addition of soluble (s) CD4 (a known ligand for HIV gp120) to DC-CD4(+) T cell cocultures restored T cell proliferation in a dose-dependent manner. By contrast, addition of antiretroviral drugs did not affect CD4(+) T cell proliferation. Furthermore, recombinant HIV gp120 inhibited proliferation in uninfected cocultures of allogeneic DC and CD4(+) T cells, an effect that was also reversed by addition of sCD4. In summary, we show that HIV gp120 produced by DC infected by HIV in vitro impairs normal CD4(+) T cell function and that sCD4 completely reverses HIV gp120-mediated immunosuppression. We hypothesize that HIV-infected DC may contribute to impaired CD4(+) T cell-mediated immune responses in vivo and that agents that block this particular immunosuppression may be potential immune adjuvants in HIV-infected individuals.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/HIV Envelope Protein gp120,
http://linkedlifedata.com/resource/pubmed/chemical/HIV Protease Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Isoantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Reverse Transcriptase Inhibitors
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
170
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4260-6
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:12682260-Adult,
pubmed-meshheading:12682260-Antigen Presentation,
pubmed-meshheading:12682260-Antigens, CD4,
pubmed-meshheading:12682260-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12682260-Cell Division,
pubmed-meshheading:12682260-Cell Separation,
pubmed-meshheading:12682260-Cells, Cultured,
pubmed-meshheading:12682260-Coculture Techniques,
pubmed-meshheading:12682260-Dendritic Cells,
pubmed-meshheading:12682260-Dose-Response Relationship, Immunologic,
pubmed-meshheading:12682260-Down-Regulation,
pubmed-meshheading:12682260-Flow Cytometry,
pubmed-meshheading:12682260-Growth Inhibitors,
pubmed-meshheading:12682260-HIV Envelope Protein gp120,
pubmed-meshheading:12682260-HIV Protease Inhibitors,
pubmed-meshheading:12682260-HIV-1,
pubmed-meshheading:12682260-Humans,
pubmed-meshheading:12682260-Interleukin-10,
pubmed-meshheading:12682260-Interleukin-12,
pubmed-meshheading:12682260-Interleukin-2,
pubmed-meshheading:12682260-Isoantigens,
pubmed-meshheading:12682260-Lymphocyte Activation,
pubmed-meshheading:12682260-Recombinant Proteins,
pubmed-meshheading:12682260-Reverse Transcriptase Inhibitors,
pubmed-meshheading:12682260-Solubility,
pubmed-meshheading:12682260-Up-Regulation
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pubmed:year |
2003
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pubmed:articleTitle |
Decreased stimulation of CD4+ T cell proliferation and IL-2 production by highly enriched populations of HIV-infected dendritic cells.
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pubmed:affiliation |
Dermatology Branch and Experimental Retrovirology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article
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