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)

F(ab')2 antibody fragments of heteroantisera directed against p28,33 (or 'Ia-like') antigen, T-cell antigen(s) (T), myeloid antigen (M), and immunoglobulin have been used along with rosetting techniques to analyse the antigenic heterogeneity of 'null' or 'unclassified' lymphoid cells purified 'negatively' from human blood by E rosette depletion of T cells and B removal on an anti-immunoglobulin immunoabsorbent. The results confirm that considerable heterogeneity exists within the 'null' cell population; the majority of cells are p28,33+ and Fcgamma-receptor-positive, and a proportion but not all of these p28,33+, Fcgamma+ cells are also C3-receptor-positive but negative for the other heteroantigens (T and M). 2-6% were 'pre-B' by the criteria of immunofluorescent staining for cytoplasmic IgM in the absence of detectable cell surface Ig. 1-3% stained intensely with anti-IgM, anti-IgG or anti-IgA, or anti-k plus anti-lambda and were presumed to be plasma cells or their immediate precursors. No null cells stained with antibody to terminal deoxynucleotidyl transferase enzyme, a marker for early T lineage cells, and less than 1% expressed an acute ('non-T, non-B') lymphoblastic-leukaemia-associated membrane antigen which is believed to be an 'early' lymphoid lineage differentiation marker. A minor subpopulation made sheep 'E' rosettes, and another made mouse 'E' rosettes after neuraminidase pretreatment of the lymphoid cells. A small proportion of 'lymphoid', 'null cells' were reactive with an anti-myelomonocytic (M) antibody. It is suggested that 'null' lymphoid cells in blood are heterogeneous and that most are not immature T or B precursors but either a relatively mature B lymphocyte population with a very low density of membrane immunoglobulin or a distinct non-T, non-B cell type.
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PMID:Phenotypes of 'null' lymphoid cells in human blood. 8 11

Cell lines obtained by in vitro transformation of bone marrow with Abelson murine leukemia virus (A-MuLV) can be divided into three classes: producers, releasing reverse transcriptase-containing particles and infectious virus; nonproducers, releasing no viral particles; and defective producers, the most common phenotype, releasing particulate reverse transcriptase in the absence of infectious virus. When such cell lines were analyzed 1 to 2 weeks after their isolation, however, all produced infectious virus. Because these cell lines were carried in culture, many ceased to release infectious virus but produced defective virions. One defective producer, SWR4, has been extensively studied. The particles it produces have the same density as that of virions of Moloney murine leukemia virus (M-MuLV). The particles contain no 35 to 70S RNA, as determined by analysis of [3H]uridine-labeled particles, and exhibit no endogenous reverse transcriptase activity. Although the reverse transcriptase enzyme is of normal size, the major structural protein of the defective virions has a molecular weight of 28,000 (p28), in contrast to the p30 of M-MuLV, and no viral glycoprotein was evident. The defective particles do not appear to arise either from the helper virus or from Abelson virus. An alteration of the protein of the helper virus is an unlikely source of p28 because particles produced by lymphoid cells transformed with another strain of M-MuLV as helper (M-MuLV-TB) contained p28 with an unaltered cleavage pattern, although M-MuLV-TB p30 differs from M-MuLV p30. The A-MuLV genome lacks the capacity to code for the reverse transcriptase virions. Clones of fibroblasts infected with A-MuLV only occasionally produce defective particles. The defective particles therefore probably arose from an endogenous virus that is preferentially expressed in the class of lymphoid cells transformed by A-MuLV. This interpretation implies that the majority of A-MuLV-transformed lymphoid cells completely lose expression of the helper virus genome.
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PMID:Virus production by Abelson murine leukemia virus-transformed lymphoid cells. 9 Jan 75

A cell line (BsT) established from neoplastic embryonal tissues of the platyfish (Xiphophorus maculatus) released spontaneously retrovirus-like particles. The particles have a buoyant density of 1.16 g/ml, a mean diameter of 100 nm and the morphology of immature retroviruses. The particle-associated proteins p70, p65, and p28 react with an antiserum directed against the major internal feline leukemia virus structural protein p27. The particles are associated with a reverse transcriptase. The purified enzyme has a molecular weight of about 70 kDa and prefers the template primers poly(rA):oligo(dT), poly(dC):oligo(dG), and poly(rC):oligo(dG) in the presence of Mn2+. The enzyme activity is inhibited by antibodies directed against the reverse transcriptase of feline leukemia virus and simian sarcoma virus. The particles contain a ribonucleic acid of about 70 S. In an endogenous reverse transcriptase reaction nucleic acids in the range of 0.2 to 0.4 kb were synthesized. In Northern blots with these nucleic acids as probe, three transcripts of about 8.5, 4.2, and 1.5 kb were detected in BsT cells. Southern blot analysis with the same probe demonstrates related sequences in the DNA of BsT cells and the platyfish and swordtail (Xiphophorus helleri). Hybridization experiments with the LTR-gag region of the feline leukemia virus show homologous sequences in the Xiphophorus genome.
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PMID:Isolation and characterization of a retrovirus from the fish genus Xiphophorus. 137 84

A human T-cell line producing human T-cell leukemia virus type I (HTLV-I), MT-2, was injected intravenously into female F344 rats aged 5 weeks to make HTLV-I carrier rats. Antibody against HTLV-I was detected at the 5th week after MT-2 injection, and its titer reached a high plateau which continued from the 15th to the 27th week. The antibodies were against p19, p24, p28 and p53 of HTLV-I antigens from MT-2 cells. The gag, pX and LTR nucleotide sequences of HTLV-I provirus were demonstrated by using polymerase chain reaction (PCR) in the peripheral-blood mononuclear cells of 3 rats at the 44th week and 2 at the 66th to 68th week out of 8 F344 rats injected with MT-2 cells. Quantification of the HTLV-I proviral sequence revealed that 30 to 60 molecules were present in 10(5) peripheral-blood mononuclear cells, indicating that the rats were chronically infected with HTLV-I. HTLV-I-infected rats could serve as a small-animal model for studying the pathophysiological state of HTLV-I carriers and also that of HTLV-I infection on various HTLV-I-related diseases, including adult T-cell leukemia and HTLV-I-associated myelopathy.
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PMID:Infection of rats with HTLV-1: a small-animal model for HTLV-1 carriers. 168 81

To determine the heterosexual spread of human T-cell leukemia virus (HTLV-I) infections, a cohort of 472 individuals with more than 5 heterosexual partners in the 6 months before entry was studied. They were recruited from visitors to the Clinic for Sexually Transmitted Diseases of the Municipal Health Service. Half of the study group was born in the Netherlands, 13% in Surinam or the Dutch Antilles, and 8% in Turkey or Morocco. Seventy percent were involved in commercial sex. Three persons were positive for HTLV-I, with serum antibodies against p19, p24, p28, gp46, and gp61 in Western immunoblot (WIB) and radio-immunoprecipitation assay (RIPA). Two of them originated from Surinam and the third was a Dutch woman. Two other individuals were HIV-positive, 19% had hepatitis B virus (HBV)-markers and 6% Treponema pallidum reacted in the hemagglutination assay (TPHA). It is concluded that HTLV-I circulates in the Surinamese population in Amsterdam and there was no evidence of appreciable heterosexual transmission.
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PMID:Prevalence of human T-cell leukemia virus antibody among heterosexuals living in Amsterdam, The Netherlands. 228 Feb 59

Cocultivation of spleen cells, lymph node cells, and thymocytes of female Wistar-King-Aptekman rats with short-term cultured male adult T cell leukemia (ATL) cells in the presence of 5-bromo-2'-deoxyuridine (BudR) resulted in the establishment of rat lymphoid cell lines, TARS-1, TARL-2, and TART-1. Cytogenic analysis of the three cell lines showed a female rat karyotype with 42 chromosomes. The surface phenotypes of TARS-1 and TART-1 were those of rat T cells. TARL-2 was only positive for rat Ia and leukocyte common antigens and brain associated T antigen. The cell lines continuously produced a type C retrovirus, human T cell leukemia virus-I (HTLV-I) and expressed ATL-associated antigens. By using monoclonal antibodies for rat IL-2 receptors, FACS analysis demonstrated that three rat T cell lines unequivocally expressed rat IL-2 receptor. TARS-1 and TART-1 but not TARL-2 were transplantable into newborn syngeneic rats and nude mice. By injecting MMC-treated TARS-1 into newborn syngeneic rats, HTLV-I carrier rats were obtained which showed gradual increase of anti-ATLA antibody titer by aging. No evidence of leukemia nor malignant lymphoma were observed in those carrier rats. Adult rats immunized with these rat cell lines produced antibodies specific for HTLV-I. The biochemical analysis of the antigen that reacted with rat sera revealed that they are the HTLV-I specific polypeptides, p28, p24, p19 and p15.
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PMID:[Rat lymphoid cell lines producing human T cell leukemia virus-I]. 288 Jul 89

Sera and cerebrospinal fluid (CSF) from patients with human T-cell leukemia virus type 1 (HTLV-1)-associated myelopathy (HAM) were analyzed by Western blotting, and normal human leukocytes were transformed by co-cultivation with HAM patients' leukocytes. The sera and CSF from all HAM patients formed specific bands with HTLV-1 viral proteins, including p19, p24, p28, p32, p40 and p53. After 2-3 weeks of co-cultivation, scattered foci of cell aggregates were noted on macrophage sheets. Surface markers of the transformed cells were OKT3(+), OKT4(+), OKT8(-), IL-2 receptor(+) and EBNA(-). Chromosome analysis showed a normal karyotype. HTLV-1 viral genome was integrated into DNA isolated from transformed cell lines. Electron microscopy revealed type C virus particles in transformed T-cell lines. These results indicate that peripheral leukocytes from HAM patients can transform HTLV-1-negative leukocytes and HAM patients have the potential to acquire adult T-cell leukemia in the future.
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PMID:Transformation of human leukocytes by co-cultivation with HTLV-1-associated myelopathy patients' leukocytes. 288 13

This study reports the immunohistological detection of serum antibody reacting with the basal aspect of syncytiotrophoblast of human chorionic villi, where SSAV/GaLV (simian sarcoma associated virus/gibbon ape lymphoma virus) type C retrovirus p30 related antigen was observed by an indirect immunofluorescent method using monospecific antibodies against SSAV p28 and GaLV p29. The immunoglobulin class of this antibody activity called 'the anti-basal aspect of syncytiotrophoblast (anti-BAST)', was exclusively IgM and detected in the sera of both female and male patients with SLE and other autoimmune diseases, but rarely in the sera of normal controls. Immunofluorescent absorption and blocking test revealed that anti-BAST specifically reacted with human placenta and cross-reacted with subhuman primate type C RNA retrovirus SSV/SSAV (simian sarcoma virus/simian sarcoma associated virus), but did not cross-react with ATLV (adult T cell leukaemia virus) and BaEV (baboon endogenous retrovirus). These results suggest the presence of a new antigen-antibody system for another human type C retrovirus related antigens(s) and a participation of retrovirus in autoimmune diseases.
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PMID:Serum antibody reacting with placental syncytiotrophoblast in sera of patients with autoimmune diseases--a possible relation to type C RNA retrovirus. 299 Jul 81

Three distinct monoclonal antibodies (MAbs) specific for human T-cell leukemia virus type-I (HTLV-I) core proteins with molecular weights of 24 kDa (p24), p19 or p15 were produced, characterized and compared. These antibodies were named NOR-1 (anti-p24, IgG2a), GIN-7 (anti-p19, IgG2b) and FR-45 (anti-p15, IgG2a). Immunofluorescence assay showed that they reacted specifically with methanol-fixed cells of virus-bearing cell lines, and that only GIN-7 bound, albeit weakly, to the surface of a small percentage of viable cells. Like natural antibodies to HTLV-I in human serum, GIN-7 stained the fixed cells brightly and diffusely, and gave more intense fluorescence than NOR-1 and FR-45, which stained restricted areas of the cells. NOR-1, GIN-7 and FR-45 specifically precipitated core proteins p24, p19 and p15, respectively, from a lysate of HTLV-IMT-2 labelled with 35S-cysteine. NOR-1 precipitated p53, p36, and p24, GIN-7 precipitated p53, p32, p28 and p19, and FR-45 precipitated p53, p36, and p15 from a lysate of 35S-cysteine-labelled MT-2 cells. GIN-7 also precipitated p32, p28 and p19 from a lysate of MT-2 cells, labelled by surface iodination, but NOR-1 and FR-45 did not detect any proteins in this lysate. GIN-7 also detected p28 in 3H-glucosamine-labelled MT-2 cells. Antibody binding competition assay showed that the sera of ATL patients significantly interfered with the binding of NOR-1 and GIN-7 but not with that of FR-45, to antigens of disrupted virus of MT-2 cells. This complete set of MAbs against the HTLV-I gag gene products is useful for biological and functional studies of the HTLV-I core proteins.
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PMID:Antigens related to three core proteins of HTLV-I (p24, p19 and p15) and their intracellular localizations, as defined by monoclonal antibodies. 300 Sep 53

A retrospective study was conducted to determine whether exposure to murine mammary tumor virus (MuMTV) induced MuMTV-specific serologic responses among intramural laboratory personnel. Results obtained with a panel of five purified structural proteins of the RIII mouse strain milk-derived MuMTV (gp55, gp34, p28, p18, and p12), by means of the enzyme-linked immunosorbent assay to assess antibody binding, established that MuMTV exposure resulted in highly significant increases in serologic responses to these test antigens as compared to age- and gender-matched controls without overt contact with MuMTV. Furthermore, immunoreactions to gp55 and gp34 were found not to be directed to the carbohydrate moieties of these glycoproteins. Similar results were obtained by assays of human immunoglobulin binding to Western blots of MuMTV proteins. These increased MuMTV-specific immunoreactivities, in general, were found to be related to degree and length of exposure to this virus. These results with MuMTV suggest the possibility of important human immune response differences between exposure to type B (MuMTV) and animal type C (leukemia-sarcoma) RNA tumor viruses, perhaps reflective of sensitivity to antibody dependence of complement-induced virolysis.
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PMID:Serologic responses to murine mammary tumor virus (MuMTV) in MuMTV-exposed laboratory personnel. 300 44


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