Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the production of granulocyte-macrophage colony stimulating factor (GM-CSF) by human T-lymphotropic virus type I (HTLV-I)-infected human glioma cells (KG-1-C and T98G). When glioma cells were co-cultured with HTLV-I-producing T cell lines (HCT-1 and MT-2), GM-CSF was detected in the culture supernatant. GM-CSF was produced in all the co-cultures even after several passages. In co-cultures of KG-1-C and HCT-1 cells with Millicell, the amount of GM-CSF produced in the supernatant was almost as low as in the culture of HCT-1 alone. Moreover, for co-cultures of KG-1-C and HCT-1 or MT-2 cells, the production of GM-CSF was significantly suppressed in the presence of IgG from patients with HAM. Double-label immunostaining showed that GM-CSF-producing glioma cells always were stained by a monoclonal antibody against HTLV-I p19, indicating that HTLV-I infection of glioma cells caused GM-CSF production. These data suggest that human glial cells infected with HTLV-I gain the ability to produce cytokines.
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PMID:Production of granulocyte-macrophage colony stimulating factor by human T-lymphotropic virus type I-infected human glioma cells. 815 17

The human T-lymphotropic virus type I (HTLV-I) has been recently associated with cases of tropical spastic paraparesis and human myelopathy. In order to study whether cells of neuroectodermic origin were susceptible to HTLV-I infection, a human glioma cell line T67 was exposed in vitro to HTLV-I by a cell-free method of virus transmission. The presence of HTLV-I proviral DNA was analyzed by polymerase chain reaction 3, 7, and 14 days after infection. The results showed the presence of LTR, pol, and tax sequences within glioma cell line 3 days after the infection. However after 7 and 14 days, detection of HTLV-I sequences remarkably decreased. P19 expression peaked 7 days after infection and decreased in the following week. These data provide evidence that cell-free transmission of HTLV-I results in transient infection of cells of glial origin.
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PMID:Transient HTLV-I infection of a human glioma cell line following cell-free exposure. 824 98

We isolated three monoclonal antibodies (mAbs), H3e, H11b and H16h, which were capable of inhibiting syncytium formation induced in a human T-cell line MOLT-4 or a human glioma line U251 MG by coculture with human T-cell leukaemia virus type I (HTLV-I)-positive human T-cell lines. The mAbs partially inhibited the plating of pseudotypes of vesicular stomatitis virus (VSV) bearing envelope antigens of HTLV-I. Formation of proviral DNA was also inhibited when indicator cells were treated with the mAbs before adsorption of HTLV-I, but not after its adsorption. They did not inhibit syncytium formation induced by human immunodeficiency virus type 1. Flow cytometry revealed that H16h hardly reacted with various HTLV-I-positive T cells, while H3e and H11b reacted with HTLV-I-positive human cells as well as HTLV-I-negative human cells. H11b and H16h immunoprecipitated the membrane antigen with a molecular weight of 20 and 110-130 kDa, respectively. Western blot analysis showed that H3e, H11b and H16h bound to the protein of 20, 20 and 110-130 kDa, respectively. Thus, these findings suggest that the 20- and 110-130-kDa cell surface proteins may play a role at the early stage of HTLV-I infection.
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PMID:Identification of membrane antigens important for adsorption of human T-cell leukaemia virus type I. 992 14