Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study describes the establishment of T-cell lines from the peripheral blood of two Bloom syndrome (BS) patients and one healthy female by co-cultivation with a lethally irradiated human T-cell line (MT-2) carrying adult T-cell leukemia (ATL) virus (ATLV). The cell lines from normal and BS subjects exhibited cell surface markers compatible with T-cell origin, and BS T-cell lines retained the original cytogenetic characteristics of the syndrome. Even though phytohemagglutinin-stimulated BS lymphocytes from the two BS patients studied all showed high levels of sister chromatid exchange (SCE), one of the BS T-lines retained the high SCE level in 100% of the cells and the other BS T-line contained two populations, one with high SCE (70%) and the other with normal SCE (30%), at a relatively constant frequency over 6 months. Transformation of normal and BS cells by cocultivation with MT-2, which carries ATLV, did not cause karyotypic changes over 6 months. ATLV infection, chromosome instability, karyotypic abnormality and SCE in BS T-lymphocytes are also discussed.
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PMID:Transformation of Bloom syndrome T-lymphocytes by cocultivation with a lethally irradiated human T-cell line carrying type C virus particles. 630 51

Mouse monoclonal antibody to HTLV p19 was used to locate HTLV p19 on the surface of cells and virions by immunofluorescence microscopy (IFM) and immunoelectron microscopy (IEM). When HTLV-producing cells HUT 102 (B2 clone), MT-2 and strain A were used as target cells, HTLV p19 was detected on the surface of cells and virions as spots or small sectors by both IFM and IEM. Cells infected with animal type-C retroviruses, e.g., gibbon ape leukemia virus, simian sarcoma virus, feline leukemia virus, and Gross murine leukemia virus, were completely negative for HTLVp19 expression. Other human T cells not producing HTLV, including HUT78 and HSB2-0, immature or pre-T cells (Molt-3) derived from leukemia patients, and fresh peripheral blood T cells from healthy persons, were also negative. In addition, B cells including Rob-B, IM-9, Raji, and BT-1 did not react with the monoclonal antibody to HTLV p19. In the light of the presence of HTLV p19 in the periphery of acetone-fixed HTLV-producing cells as shown by IFM, it seems most likely that HTLV p19 is an internal antigen of HTLV with part of its structure protruding out of the viral and cell membrane. The monoclonal antibody to HTLV p19 did not lyse HTLV-producing cells in the presence of complement, as expected, because the antibody is an IgG1. Antibody-dependent cell-mediated cytotoxicity was also studied by the 51Cr-release assay. No cytotoxicity was observed. Although HTLV p19 does not contribute to the destruction of malignant T cells for treatment and/or virions for prophylaxis, this protein is an important marker for diagnosis of HTLV infection. The patterns of HTLV p19 expression described above were exactly the same for American HTLV-producing HUT 102 (B2 clone), for strain A cells and for Japanese HTLV-producing MT-2 cells. These results further substantiate the close relationship of the Japanese and American HTLV isolates.
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PMID:Location of human T-cell leukemia virus (HTLV) p19 antigen on virus-producing cells. 631 98

Experimental transmission of adult T-cell leukemia (ATL) virus (ATLV) into human B lymphocytes was attempted. Cocultivation of B-cell rich fraction of peripheral blood from a healthy adult with X-ray irradiated ATLV producer MT-2 cells resulted in the establishment of OKA(B) cell line co-infected with both Epstein-Barr virus (EBV) and ATLV. OKA(B) cells and its subclones contained: (1) B cell markers exclusively; (2) both EBV-specific antigen, EBNA and ATLV-specific antigen, ATLA detected by immunofluorescence test; (3) ATLV-specific polypeptides, p24 and p19; (4) ATLV-specific mRNA in ATLA-positive clones; (5) ATLV and EBV particles detectable by electron microscopy. These data clearly show that human B lymphocytes are susceptible to ATLV infection.
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PMID:In vitro infection of human B lymphocytes with adult T-cell leukemia virus. 632 Oct 19

A human type-C retrovirus, designated HTLV (human T-cell leukemia virus), was isolated from the HTLV producer cell line MT-2. Agarose gel electrophoresis analysis 32P-labeled HTLVMT-2 virion RNA revealed that HTLVMT-2 virion RNA consists mainly of 24S and small amounts of 35S and 32S RNAs. The 24S HTLVMT-2 virion RNA and unfractionated HTLVMT-2 virion RNA were translated in a rabbit reticulocyte lysate system in vitro. The predominant polypeptide synthesized from 24S RNA had an apparent mol. wt. of 28 000 (28 K); unfractionated HTLVMT-2 virion RNA directed the synthesis of 53 000 (53 K), 33 000 (33 K) and 28 000 (28 K) polypeptides as main components. Most of the polypeptides synthesised in vitro by translation of HTLVMT-2 virion RNAs possess the same sizes as the proteins formerly designated as ATLA (ATL-associated antigen) in SDS-polyacrylamide gel electrophoresis and immunologically precipitated with sera of ATL patients. Therefore, the antigens termed ATLA, found by the serological study of ATL, are HTLVMT-2 encoded polypeptides.
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PMID:Translation of HTLV (human T-cell leukemia virus) RNA in a nuclease-treated rabbit reticulocyte system. 632 67

Peripheral blood lymphocytes from a Japanese monkey (Macaca fuscata) were co-cultivated with lethally irradiated MT-2 cells that carry abundant type C virus particles (ATLV) isolated from a patient with adult T-cell leukemia (ATL). After six weeks, a lymphoid cell line designated Si-1 was established from the simian lymphocytes. The Si-1 line was E-, SIg-, Leu-1-, OKI1+, EBNA-, ATLA+ and ATLV+. Co-cultivation of peripheral blood lymphocytes from three anti-ATLA positive and two negative healthy adults resulted in the establishment of three lymphoid cell lines derived either from an anti-ATLA positive donor or both donors. All three cell lines were E+, SIg-, Leu-1+, OKI1+, EBNA-, ATLA+ and ATLV+. This mixed lymphocyte culture technique provides a simple means for the isolation of ATLV from healthy ATLV carriers.
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PMID:[Establishment and characterization of ATLV-producing cell lines]. 634 44

Adult T-cell leukemia-associated antigen (ATLA) and adult T-cell leukemia virus (ATLV) antigens were localized in the MT-2 cell system by the immunocolloidal gold method using 71 human sera having various anti-ATLA titers and rabbit anti-ATLV antisera. In the thin-section method with anti-ATLA-positive human sera and rabbit antisera, protein A-gold particles were preferentially observed on and around sectioned adult T-cell leukemia (ATL) virions located in pericellular aggregates and within the cytoplasmic vacuoles but nowhere else in a significant number. The number of gold particles per ATL virion was statistically well correlated with the anti-ATLA titers of human sera applied (p less than 0.005). The preembedding method showed that pericellular ATL virions were specifically tagged with protein A-gold, but the antigens in question were not expressed on the plasma membrane of MT-2 cells. The absence of ATLA and ATLV antigens on the plasma membrane constitutes a unique pathobiological feature of ATL and ATLV as compared with other retrovirus systems.
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PMID:Localization of adult T-cell leukemia-associated antigens by the immunocolloidal gold method. 643 May 51

A T-cell line, MT-2, derived from human cord blood lymphocytes by cocultivation with adult T-cell leukemia (ATL) cells is a continuous producer of type-C virus particles. Electron microscopy of MT-2 cells cultured for 1-3 weeks in medium containing 10% ATL patients' sera revealed agglutination of type-C virus particles within the electron-dense deposits in the extracellular spaces. No such agglutination occurred in control cultures supplemented with normal human or fetal calf serum. These results provide direct evidence for the specific reactivity of ATL patient's sera with type-C virus particles in the MT-2 cell line at the ultrastructural level.
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PMID:Immunoagglutination of type-C virus particles in a human T-cell line by serum supplementation from patients with adult T-cell leukemia. 660 Nov 6

Sera from patients with adult T-cell leukemia (ATL) or other diseases and from healthy adults, whose titers of antibodies against ATL-associated antigens (ATLA) had been determined by indirect immunofluorescence, were analysed by a procedure of immunoprecipitation followed by SDS-polyacrylamide gel electrophoresis. For this an ATL virus (ATLV)-producer cell line, MT-2, was labelled with [35S]-methionine. All 12 anti-ATLA-positive sera but none of the eight anti-ATLA-negative sera tested reacted specifically with four polypeptides with molecular weights of 70,000, 53,000, 36,000 and 24,000 daltons. Furthermore, enrichment of three polypeptides with molecular weights of 76,000, 43,000 and 28,000 daltons was observed on reaction with anti-ATLA-positive sera. In control experiments using ATLA-negative T-cell lines, Molt-4 and HPB-ALL, none of these seven polypeptides were precipitated by reaction with anti-ATLA-positive sera. All six anti-ATLA-positive sera tested were shown to react with a polypeptide with a molecular weight of 24,000 of purified ATLV.
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PMID:Antigens in an adult T-cell leukemia virus-producer cell line: reactivity with human serum antibodies. 675 45

We have tried to isolate a retrovirus from adult T-cell leukemia (ATL) which is a new clinical entity of T-cell malignancy. This disease shows a peculiar geographic clustering of patient birthplaces in the southwestern part of Japan. A retrovirus was isolated from the T-cell line, MT-2, which was established from cord lymphocytes cocultivated with leukemic cells from an ATL patient and characterized by: (a) density of 1.152-1.155 g/ml in sucrose gradient; (b) reverse transcriptase activity; (c) specific protein components; (d) RNA labeled with 3H-uridine, and (e) specific DNA complementary with viral RNA. The retrovirus was named adult T-cell leukemia virus (ATLV). Complementary DNA (cDNA) prepared by the endogenous reaction of detergent-treated virions hybridized with 35S RNA in MT-2 cells and another ATL cell line, MT-1, and this 35S RNA was inducible with IUDR treatment of the MT-1 cells, indicating that ATLV is a typical retrovirus containing 35S RNA as the genome. However, the cDNA did not show any detectable hybridization with cellular RNA of other human cell lines unrelated to ATL. The ATLV proviral DNA was detected in the chromosomal DNA of MT-1 and MT-2 cell lines as well well as in fresh peripheral blood cells of all five patients with ATL tested; however, it was not found in those of three healthy adults. Furthermore, sera from the patients reacted with one component of the ATLV protein, but normal sera did not. These sera and all other sera from ATL patients were previously shown to react with antigen(s) in leukemic cells of ATL, and the antigen(s) also reacted with sera from about 25% of the healthy adults in the endemic area, but not in the non-endemic area. These close associations of ATLV proviral DNA and proteins with ATL are direct evidence strongly suggesting the involvement of the retrovirus, ATLV, in the leukemogenesis of human ATL.
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PMID:A retrovirus from human leukemia cell lines: its isolation, characterization, and implication in human adult T-cell leukemia (ATL). 698 2

Cyclopentenone prostaglandins PGA1 and PGJ2 can inhibit the growth of HTLV-1 infected cord blood-derived human mononuclear cells (CBMC), both after acute infection and in chronically infected, immortalized cells. When CBMC were exposed to HTLV-1 infection by coculturing with lethally irradiated, virus-donor allogeneic MT-2 cells, they underwent a proliferative response, that peaked within the first week and then declined. PG treatment did not inhibit the initial proliferation (day 4) of cocultured CBMC, while multiple treatments with PGA1 and more efficiently with PGJ2, suppressed the late cell proliferation (from day 8 onward). The pharmacological effects of PGA1 and PGJ2 were reversible and therefore multiple treatments were required to maintain their antiproliferative activity. Increasing concentrations (20, 40, 80 IU/ml) of recombinant IL-2 did not affect the virus-associated proliferative response of CBMC, and exogenous IL-2 did not revert the antiproliferative effect of both PGs. Arrest of proliferation in cocultured CBMC occurred concomitantly with expression of high levels of HSP70 in the cells. In fact, though HSP70 expression was induced early (day 5) after exposure to HTLV-1, its expression was further increased after multiple PG treatments and high levels were found when the antiproliferative effect of PGs became manifest. Since HSP70 protein family is involved in the control of cell cycle as well as in antigen processing and presentation during the immune response against tumor cells and pathogens, the persistent expression of this protein in PG-treated cocultures suggested that, beside inhibiting the growth of virus-infected cells, HSP70 expression might play a role in modulating the immune function of CBMC. However, unlike in most virus infection models, in which cyclopentenone PGs exert clear antiviral effects by inhibiting the synthesis and maturation of virus proteins, no antiviral activity was found in this model of infection. This strongly suggests that the main effect of these PGs against HTLV-1 infected cells consists in inhibiting proliferation in vitro without affecting viral expression.
Leukemia 1994 Jun
PMID:Antiproliferative activity of cyclopentenone prostaglandins in early HTLV-1 infection is independent of IL-2 and is associated with HSP70 induction. 751 27


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