Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04141 (granulocyte-macrophage colony-stimulating factor)
 6,790 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of placental cells in transplacental transmission of human immunodeficiency virus type 1 (HIV 1) was investigated. Placental macrophages and trophoblasts, which together represent the main cell components of the placenta, were cultivated separately and then compared to foetal monocyte-derived macrophages for susceptibility to HIV 1 infection. Placental macrophages treated with granulocyte-macrophage colony-stimulating factor (GM-CSF) were less easily infected with HIV 1 than were GM-CSF-treated foetal monocyte-derived macrophages. HIV 1 replication in cocultures consisting of infected placental macrophages together with a highly HIV 1-permissive cell line (CEM) was detected persistently for at least 6 weeks by reverse transcriptase assay, even though placental macrophages expressed no detectable CD4 receptor, as indicated by indirect immunofluorescence. HIV 1-specific DNA sequences were also detected in infected placental macrophages. Trophoblasts exhibited no detectable CD4 expression and did not support the replication of HIV 1, although low levels of HIV 1-specific DNA sequences could be detected in infected trophoblasts. Placental macrophages or trophoblasts (or both) may thus play an important role in transplacental HIV 1 transmission.
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PMID:Replication of human immunodeficiency virus type 1 in primary cultured placental cells. 189 50

In this study, we evaluated the effect of a short-term exposure (2 hours) to two different lymphocytotropic strains of human immunodeficiency virus type 1 (HIV-1; HIVIIIB and ICR-3) on the survival of a factor-dependent CD34+ hematopoietic progenitor cell line (TF-1). At flow cytometry analysis, a significant (P < .05) increase in the frequency of apoptotic cell death was observed in HIV-1-treated TF-1 cells, supplemented with low doses of either interleukin-3 (IL-3; 0.02 to 1 ng/mL) or granulocyte-macrophage colony-stimulating factor (GM-CSF; 0.02 to 0.2 ng/mL) with respect to mock-treated cells. On the other hand, higher doses of both cytokines or combinations of suboptimal concentrations of IL-3 plus GM-CSF (eg, 0.2, plus 0.2 ng/mL) completely reversed the HIV-1-induced increase of apoptosis. Remarkably, no signs of productive or latent virus replication were ever observed in HIV-1-treated TF-1 cells up to 16 days of liquid culture. In parallel experiments, the in vitro exposure to HIVIIIB induced a significant and progressive increase of apoptotic death in purified bone marrow CD34+ cells, seeded in liquid cultures in the presence of 1 ng/mL IL-3. The HIV-1-induced apoptosis of TF-1 cells was likely triggered by the simple interaction of HIV-1 envelope glycoprotein gp120 with CD4 receptor, which was expressed at a low level on the surface of TF-1 cells. In fact, treatment of TF-1 cells with recombinant gp120 plus a polyclonal anti-gp120 antibody or with anti-CD4 monoclonal antibody plus rabbit antimouse IgG significantly increased the percentage of apoptotic death. These data suggest that HIV-1, and perhaps also free gp120 in the presence of anti-gp120 antibody; could play a direct role in the pathogenesis of peripheral blood cytopenias in acquired immunodeficiency syndrome patients by inducing apoptotic death of hematopoietic progenitor cells without the need of a direct infection.
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PMID:In vitro exposure to human immunodeficiency virus type 1 induces apoptotic cell death of the factor-dependent TF-1 hematopoietic cell line. 750 78