Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral blood mononuclear cells obtained during recrudescent Herpes simplex virus (HSV) infection and stimulated with UV-inactivated viral antigen (UV-HSV) for 24 hr produced a low molecular weight (dialyzable) factor that inhibited lymphokine activity. This factor prevented the expression of leukocyte inhibitory factor (LIF) activity, but not its production. It was not made in UV-HSV-stimulated cultures grown in presence of 2 X 10(-6) M indomethacin nor in cultures of peripheral blood mononuclear cells obtained during convalescence or quiescence (greater than 4 days from onset of clinical symptoms) or from seropositive controls without a history of recurrent HSV disease. Dialyzable inhibitory factor production required OKM1+, OKT8+, and OKIa+ cells as determined by complement-mediated lysis with monoclonal antibody. Dialyzable inhibitory factor activity was associated with a trypsin-sensitive 8.2 K fraction as determined by Sephadex chromatography followed by sodium dodecyl sulfate-acrylamide gel electrophoresis.
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PMID:Reactivation of herpes simplex virus is associated with production of a low molecular weight factor that inhibits lymphokine activity in vitro. 302 76

Spontaneous small polykaryocytes were detected in a cell line designated BJ-o that harbors the BamHI J fragment of herpes simplex virus 1 DNA and expresses constitutively glycoprotein D (gD). The fusion activity of BJ-o cells correlated with gD production and was drastically reduced following exposure of the cells to monoclonal antibody HD1 to gD. Studies on the characteristics and requirements of cell fusion dependent on gD led to the conclusion that the characteristics and requirements for gD-mediated fusion activity of BJ-o cells are similar to those previously reported for cell fusion induced by the virus in that (i) polykaryocytosis was not augmented by exposure to medium of low pH with or without prior exposure to trypsin, (ii) the number of polykaryocytes was reduced following removal of terminal sialic acid residues by neuraminidase, and (iii) the number of polykaryocytes was augmented by masking of high-mannose N-linked oligosaccharides with concanavalin A or with its reduced form, succinyl concanavalin A. This effect was reversed by competition with mannose.
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PMID:Herpes simplex virus glycoprotein D is sufficient to induce spontaneous pH-independent fusion in a cell line that constitutively expresses the glycoprotein. 305 54

Trypsinization of normal human diploid cells (WI-38 and MRC 5) resulted in the appearance of complement-fixing reactivity with an immunoglobulin (anti-HeLa G globulin), prepared against a purified HeLa (malignant human) cell antigen (G), which reacts with various malignant human cell lines and tumors but not with certain normal human cells. The presence of receptors in the nonreacting, untrypsinized normal human cells and the specificity of the reactive groups that appeared after trypsinization was established by the fact that the antibody could be completely absorbed with large quantities of packed, untrypsinized human cells but not with similar quantities of either rabbit or guinea-pig kidney tissue-culture cells, which did not react with this antibody either before or after treatment with trypsin. The change produced by trypsinization is thus similar to the previously demonstrated appearance of reactive groups with the same anti-HeLa G globulin in normal human cells at certain times after infection with herpes simplex and vaccinia viruses. The fact that the trypsinized WI-38 cells absorbed more antibody than the same number of cells before trypsinization indicated that trypsinization resulted not only in the appearance of reactivity with antibody but also in a greater concentration of combining receptors, which is unlike the situation with lectins producing agglutinability without an increase in the number of receptors. Moreover, the fact that absorption with trypsinized normal cells removed larger amounts not only of the antibody reacting with the trypsin-treated WI-38 cells but also of antibody that reacts with WI-38 cells infected with herpes simplex virus and with the malignant HEp-2 cells, suggests that the combining groups that emerge after trypsinization of the normal human cells are the same or similar to those present in malignant human cells (HEp 2) and to those that emerge after infection of the normal human cells with herpes simplex virus.
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PMID:Appearance in trypsinized normal cells of reactivity with antibody presumably specific for malignant cells. 434 82

Human epidermis was separated from dermis by means of a suction blister device and dissociated with trypsin. The epidermal cell (Ec) suspensions contained 2-6% Langerhans cells (Lc). Using a new rosette technique for enrichment of Lc, suspensions were obtained that contained 50-92% viable Lc. Ec, enriched Lc, or peripheral blood monocytes (Mo) were cocultured with or without antigens (Candida albicans, herpes simplex virus) and autologous T lymphocytes from sensitized donors. Strong proliferative T-cell responses were obtained provided Ec, enriched Lc, or Mo were also present. Furthermore, Lc were more effective than similar numbers of Mo in inducing T-cell responses to the antigens tested, and Lc did not require the presence of significant numbers of keratinocytes to exert this function.
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PMID:Enriched epidermal Langerhans cells are potent antigen-presenting cells for T cells. 609 May 38

The effects on human chromosomes of types 1, 2 and of intermediate serotype of herpes simplex virus (HSV) was compared in fibroblast and lymphocyte cultures. The karyological changes due to HSV were shown to depend on the serotype used as well as on the kind of cells examined (agent-specificity and cell-reaction specificity). Differences were noted among the strains in relation to the degree and character of the aberrations induced. Conventional Giemsa staining and the trypsin G-banding techniques were used to localize aberrations in the length of human fibroblast and lymphocyte chromosomes after HSV infection. A non-random damage of chromosomes 1 and 3 displaying the same pattern in either cell type was established. The distribution of chromosomal abnormalities was independent of the chromosome length. The topographic banding analysis of lesions induced by strains of HSV-1, HSV-2 and intermediate serotypes showed that the most frequent aberrations were localized in bands p32, p34, q21 and q32 of chromosome 1 and in the band q21 of chromosome 3. The localization of the most frequently occurring aberrations in the chromosomes belonging to other groups was also determined.
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PMID:Effects of herpes simplex virus strains on human fibroblast and lymphocyte chromosomes and the localization of chromosomal aberrations. 614 51

Epidermis from patients suffering from recurrent herpes labialis was separated from dermis by means of a suction blister device and dissociated with trypsin. The epidermal cell suspensions obtained were 80--95% viable and contained 3--5% Langerhans' cells, as judged by immunofluorescence staining of the cells with a rabbit anti-DR antiserum. T lymphocytes from the same patients were co-cultured with herpes simplex virus antigen (HSV-Ag) or live virus (HSV), with or without epidermal cells or macrophages. A strong proliferative T cell response to HSV-Ag and HSV was obtained, provided that the cultures also contained epidermal cells or macrophages. Pretreatment of the epidermal cells with a rabbit anti-DR antiserum plus complement abolished the responses, while pretreatment with normal rabbit serum plus complement did not. These data therefore indicate that HLA--DR positive Langerhans' cells are able to present herpes simplex virus in an immunogenic way to T lymphocytes.
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PMID:Studies on human epidermal Langerhans' cells: II. Activation of human T lymphocytes to herpes simplex virus. 616 7

The nature of the refractoriness of C6 glioblastoma cells to herpes simplex virus type I (HSV-I) infection has been studied. The cells were restricted in susceptibility to HSV-I since only a small proportion of the cells could be infected by HSV-I and the virus yield per cell was low. The susceptibility to infection was increased by treating the cells with trypsin-EDTA prior to infection. The cells so treated recovered resistance to the virus when incubated at 37 degrees C, their resistance being restored to the initial level in 2 days. This restoration was inhibited by addition of cycloheximide or puromycin. Trypsin-EDTA treatment of C6 cells increased the efficiency of adsorption of HSV-I and the formation of stable cell-virus complexes from which the virus could not be dissociated by heparin.
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PMID:Stimulation of herpes simplex type I infection of C6 cells by trypsin-EDTA. 624 84

The formation of glucosamine-containing cell surface glycoproteins of herpes simplex virus (HSV) infected BMK cells was studied. Tunicamycin (TM) and 2-deoxy-D-glucose (DG) were used as inhibitors. With both inhibitors the multiplication of HSV was inhibited. DG markedly reduced cellular uptake of radioactively labelled glucosamine while TM interfered with the processing of glucosamine into TCA-insoluble material. Gel filtration chromatography on Sephadex G50 gel of cell surface material released by trypsin and further prepared by digestion with pronase indicated that TM and DG reduced the apparent high molecular weights of virus induced surface glycoproteins. In presence of DG the accumulation of a class of glucosamine-containing heterosaccharides (MW less than 3000) not present on DG-free HSV infected cells was observed. In TM treated cells virtually all surface heterosaccharides with molecular weights exceeding 3000 and containing glucosamine disappeared. Moreover, a component compatible with a lipid-linked oligosaccharide present in DG treated cells was not observed in HSV infected TM treated cells. The results exemplifies some different steps in glucosamine metabolism of virus induced cell surface glycoproteins differently affected by tunicamycin and 2-deoxy-D-glucose.
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PMID:Glucosamine metabolism of herpes simplex virus infected cells. Inhibition of glycosylation by tunicamycin and 2-deoxy-D-glucose. 625 82

Mice intraperitoneally inoculated with a sublethal dose of herpes simplex virus (HSV) produced immunoglobulin G antibody-dependent cellular cytotoxicity (ADCC) and radioimmunoassay (RIA) antibody as early as 3 days after infection. There was a rise in natural killer cytotoxicity (NKC) to infected and uninfected target cells 1 to 3 days postinfection mediated by nonadherent peritoneal cells (PC) in mice inoculated with HSV, but also with other substances commonly used in tissue culture media. HSV caused the highest and most consistent increase in NKC. PC-NKC, as ADCC, was inhibited by latex and silica, both macrophage inhibitors. PC-ADCC markedly declined 3 to 8 days after HSV inoculation. This was not due to a soluble or cellular suppressor factor, was not reversed by incubation or trypsin treatment of PC, was not associated with a change in PC Fc receptors, adherence, or acridine orange staining characteristics, and could not be induced by inactivated HSV. In vitro inoculation of PC with HSV similarly caused a reduction in the ability of PC to mediate ADCC to HSV-infected target cells. These data demonstrate the complex stimulatory and inhibitory interactions between virus and host defense mechanisms.
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PMID:Effect of herpes simplex virus infection on murine antibody-dependent cellular cytotoxicity and natural killer cytotoxicity. 626 Jun 74

The expression of herpes simplex virus (HSV) type-common surface antigens (CSA) in a representative cell clone (155-4-03) of hamster cell line 155-4 transformed by HSV type 2 was enhanced by treatment with inhibitors of RNA synthesis [adriamycin (ADM) and daunomycin] but not with inhibitors of DNA synthesis (2-iododeoxyuridine, bleomycin, mitomycin C and cytosine arabinoside), although all these drugs decreased the number of viable cells to a similar extent. ADM-enhanced CSA expression in the clone was inhibited by puromycin and 2-deoxy-d-glucose, suggesting that the enhanced expression required both protein synthesis and glycosylation. This enhanced expression was sensitive to protease inhibitors (antipain and p-nitrophenyl-p'-guanidinobenzoate) and procaine, which is known to inhibit trypsin action and the organization of cell membrane-associated cytoskeletal elements (microfilaments and microtubules). Furthermore, low concentrations of ADM (0.1 microgram/ml) and actinomycin D (0.5 microgram/ml) enhanced CSA expression additively, but the most effective concentrations of ADM (0.25 microgram/ml) and actinomycin D (2 microgram/ml) did not. These findings indicated that the two drugs enhance CSA expression in the clone by a common mechanism.
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PMID:Expression of herpes simplex virus type-common surface antigens in clonal cells of an HSV type 2-transformed line: effect of adriamycin. 627 70


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