Source:http://linkedlifedata.com/resource/pubmed/id/10580406
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
17
|
| pubmed:dateCreated |
1999-12-17
|
| pubmed:abstractText |
The ability of CD8+ T lymphocytes to suppress the transcription and replication of HIV-1 is well documented. We have demonstrated that the factor(s) responsible for the suppression of HIV-1 LTR-mediated gene expression are not the CC chemokines RANTES, MIP-1alpha, and MIP-1beta. Interestingly, these and other chemokines and cytokines are produced by both CD8+ and CD4+ T lymphocytes. On the presumption that CD4+ T lymphocytes may also be able to modulate HIV-1 expression in vitro we assessed the LTR-modulatory effects of a panel of culture supernatants derived from stimulated CD4+ T lymphocytes from HIV-positive patients and uninfected controls. Supernatants of both CD4+ and CD8+ T cells mediated a suppression of LTR-driven gene expression in Jurkat T cells and an enhancement of gene expression in U38 monocytic cells. On the basis of these results, and using a herpesvirus saimiri (HVS)-transformed CD4+ T lymphocyte clone (HVSCD4), we demonstrate that both suppressive and enhancing effects are dose dependent. Furthermore, we have shown that supernatants of both HVSCD4 and HVSCD8 cells suppress LTR-mediated gene expression and HIV-1 replication in transfected/infected T cells. In U1 monocytic cells, supernatants of both CD4+ and CD8+ lymphocytes from an HIV-1-infected individual enhanced LTR-mediated gene expression, HIV-1 replication, and TNF-alpha production. However, only these effects as induced by CD8+ T cells were sensitive to the G protein inhibitor pertussis toxin. These results indicate that factors produced by both CD4+ and CD8+ T cells exert dichotomous effects on HIV-1 gene expression and replication in T cells and monocytes.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Nov
|
| pubmed:issn |
0889-2229
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
20
|
| pubmed:volume |
15
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1553-61
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:10580406-CD4-Positive T-Lymphocytes,
pubmed-meshheading:10580406-CD8-Positive T-Lymphocytes,
pubmed-meshheading:10580406-Cell Line,
pubmed-meshheading:10580406-Cell Transformation, Viral,
pubmed-meshheading:10580406-Culture Media, Conditioned,
pubmed-meshheading:10580406-Dose-Response Relationship, Immunologic,
pubmed-meshheading:10580406-Gene Expression Regulation, Viral,
pubmed-meshheading:10580406-HIV Long Terminal Repeat,
pubmed-meshheading:10580406-HIV-1,
pubmed-meshheading:10580406-Herpesvirus 2, Saimiriine,
pubmed-meshheading:10580406-Humans,
pubmed-meshheading:10580406-Jurkat Cells,
pubmed-meshheading:10580406-Lymphokines,
pubmed-meshheading:10580406-Monocytes,
pubmed-meshheading:10580406-Pertussis Toxin,
pubmed-meshheading:10580406-Transcription, Genetic,
pubmed-meshheading:10580406-U937 Cells,
pubmed-meshheading:10580406-Virulence Factors, Bordetella,
pubmed-meshheading:10580406-Virus Replication
|
| pubmed:year |
1999
|
| pubmed:articleTitle |
T cell-derived suppressive activity: evidence of autocrine noncytolytic control of HIV type 1 transcription and replication.
|
| pubmed:affiliation |
Department of Pathology and Molecular Medicine, McMaster University Health Sciences Centre, Hamilton, Ontario, Canada.
|
| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|