| http://purl.uniprot.org/citations/10490959 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10490959 | http://www.w3.org/2000/01/rdf-schema#comment | "The pathogenesis of HIV-1 infection is influenced by the immunoregulatory responses of the host. Macrophages present in the lymphoid tissue are susceptible to infection with HIV-1, but are relatively resistant to its cytopathic effects and serve as a reservoir for the virus during the course of disease. Previous investigators have demonstrated that increased serum levels of TNF-alpha contribute to the clinical symptoms of AIDS and that TNF-alpha stimulates the production of HIV-1 in chronically infected lymphocytic and monocytic cell lines by increasing HIV-1 gene expression. Although previous studies have suggested that TNF-alpha may increase HIV-1 infection of primary human mononuclear cells, some recent studies have indicated that TNF-alpha suppresses HIV-1 infection of macrophages. We now demonstrate that TNF-alpha suppresses HIV-1 replication in freshly infected peripheral blood monocytes (PBM) and alveolar macrophages (AM) in a dose-dependent manner. As TNF-alpha has been shown to increase the production of C-C chemokine receptor (CCR5)-binding chemokines under certain circumstances, we hypothesized that TNF-alpha inhibits HIV-1 replication by increasing the expression of these HIV-suppressive factors. We now show that TNF-alpha treatment of PBM and AM increases the production of the C-C chemokine, RANTES. Immunodepletion of RANTES alone or in combination with macrophage inflammatory protein-1alpha and -1beta block the ability of TNF-alpha to suppress viral replication in PBM and AM. In addition, we found that TNF-alpha treatment reduces CCR5 expression on PBM and AM. These findings suggest that TNF-alpha plays a significant role in inhibiting monocytotropic strains of HIV-1 by two distinct, but complementary, mechanisms."xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/author | "Coffey M.J."xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/author | "Markovitz D.M."xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/author | "Strieter R.M."xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/author | "Rochford R."xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/author | "Lane B.R."xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/author | "Woodford N.L."xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/date | "1999"xsd:gYear |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/pages | "3653-3661"xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/title | "TNF-alpha inhibits HIV-1 replication in peripheral blood monocytes and alveolar macrophages by inducing the production of RANTES and decreasing C-C chemokine receptor 5 (CCR5) expression."xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://purl.uniprot.org/core/volume | "163"xsd:string |
| http://purl.uniprot.org/citations/10490959 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/10490959 |
| http://purl.uniprot.org/citations/10490959 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/10490959 |
| http://purl.uniprot.org/uniprot/P13501#attribution-19ED2B3D04545973D12C4786C917E06F | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/10490959 |
| http://purl.uniprot.org/uniprot/P01375#attribution-19ED2B3D04545973D12C4786C917E06F | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/10490959 |