Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phenotypic profile of atypical cells from a patient with cutaneous multilobated T-cell lymphoma was investigated using a multiparameter approach including evaluation of membrane markers, cytochemistry, and functional activity. Retroviral sequence restriction analysis was also used to investigate the presence of human T-cell leukaemia/lymphoma virus type I (HTLV-I) in atypical cells infiltrating the skin and in otherwise normal peripheral blood lymphocytes. The atypical cells appeared to belong to the T-lineage demonstrating OKT11 positivity, E-rosette formation, tartrate-sensitive acid phosphatase and beta-glucuronidase activity, and consistent negativity for cytoplasmic and/or surface monoclonal immunoglobulins. However, they failed to stain for other T-lymphocyte-associated antigens, such as those defined by OKT3, OKT4, OKT6, OKT8, OKT9, OKT10, Leu-2a and Leu-3a monoclonal antibodies, and did not express a definite alpha-naphthyl-acetate esterase pattern. Additional studies including phagocytosis tests and a series of monoclonal antibodies against phagocytic and natural killer cell associated antigens were all negative. No HTLV-I related sequences were found in either the cells infiltrating the skin or in circulating lymphocytes. To our knowledge, in previously reported cases of cutaneous multilobated cell lymphoma a clear T-lymphocyte phenotypic profile was demonstrated. Our present data indicate that this is not always necessarily the case. The peculiar phenotype we found might represent a transitional state between different T-cell subsets or an as yet unrecognized phenotype of a neoplastic T-lymphocyte which lacks a normal counterpart.
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PMID:Cell surface marker studies in a patient with cutaneous multilobated T-cell lymphoma. 390 11

The effects of Bestatin, a low molecular weight metabolite of Streptomyces olivoreticuli on the human and mouse/rat immune system, have been studied in detail. To describe the activity of the immunomodulating dipeptide, it has been tested in vitro, ex vivo and in vivo in various experimental models. Bestatin simultaneously applied with selected antigens to mice was able to enhance the DTH response against a challenge injection of the respective antigen given into the footpad. Serum antibody levels against those antigens were uneffected. However, an increase of PFC could be found in those mice given high doses of Bestatin. On natural killer cell activity against Yac-1 tumor cells the dipeptide had no effect in low responder (DBA2/J) mice. In high responder mice (CBA/JCr), however, a significant increase of NK cell activity of spleen cells could be found, when the drug was given on day 0 or on days 0 to 3 and the test was performed on day 4. Bestatin had no effect on the generation of allogeneic cytotoxic T-lymphocytes in vivo or in vitro and even a suppressive effect on the induction of syngeneic antitumor CTL. Contrary to this suppressive effect, Bestatin increases in the popliteal lymph node assay the weights in a dose-dependent way. When mouse macrophages or human monocytes were either incubated in vitro with Bestatin or mice were treated with the dipeptide parenterally or orally and the macrophages from those mice were investigated, Bestatin induced in vitro and in vivo a dose-dependent increase in pinocytic uptake of radioactive colloidal gold. Also the oxidative metabolism was dose-dependently augmented as measured by chemiluminescence. Bestatin modulates the macrophage mediated cytotoxicity. In vitro or in vivo activated mononuclear phagocytes exhibited a dose-dependent increase in cytotoxic activity for several tumor target cells. A minimum ratio of 50:1 effector to target cells was necessary for this cytotoxic effect. A similar degree of activation was observed in macrophages from athymic nu/nu-mice or from endotoxin resistant C3H/HeJ-mice. Other parameters of macrophage activation were determined by measuring secretion of lysosomal enzymes and liberation of prostaglandins. Bestatin interacts with macrophages in vivo and in vitro by increasing their secretory activity of acid hydrolases (beta-glucuronidase, beta-galactosidase, and N-acetyl-beta-D-glucosaminidase). This release was dose- and time-dependent and not associated with any sign of cell death. Another class of mediators produced by macrophages after stimulation with Bestatin were the prostaglandins E2 and F2a.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Studies on the mechanisms of action of the immunomodulator Bestatin in various screening test systems. 638 22

The morphology, histochemistry, cell surface antigens, and natural killer cell (NK) activity of 10 primary and 10 transplantable large granular lymphocyte (LGL) leukemias of aging F344 rats were studied. The LGL leukemia is the major cause of death of aging F344 rats. Morphologically, the LGL leukemias were composed of cells with either pleomorphic nuclei with many intracytoplasmic granules or round nuclei with few intracytoplasmic granules. The granules appeared to be lysosomes containing beta-glucuronidase and acid phosphatase and ultrastructurally developed in association with vesicles in the Golgi apparatus. Splenic natural killer cell activity against YAC-1 cells varied from case to case, and it appeared to be associated with LGL leukemia cells. Some transplantable leukemias had stable NK activity. Fluorescence-activated cell sorter (FACS) analysis of surface antigens revealed the LGL leukemias to be heterogeneous, and there was no correlation between cytotoxic activity and cell surface antigens. Although the morphologic features of cells in LGL leukemias resemble those of normal rat LGLs, differences in cytotoxic activity and surface antigens suggest that LGL tumors represent a heterogeneous group of leukemias which may serve as a model for the study of origin and lineage of normal LGL and NK cells.
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PMID:Large granular lymphocyte leukemia. A heterogeneous lymphocytic leukemia in F344 rats. 683 19

We studied the relationship between cell morphology and surface markers in three patients with granular lymphocyte proliferative disorders. In the two patients with CD3+ CD4-CD8+ cells, there were no atypical cells, and the granules were uniformly fine: In the third patient, who had CD3+ CD4+ CD8- cells, atypical nuclei and the irregular granules in in size were observed. The granules were stained with beta-glucuronidase showing localized coarse features and made clumps, in the staining pattern characteristic of granular lymphocytes. The patient with CD4- CD8+ cells showed cytotoxic T cell phenotype, and the other DN cells type (usually associated with a CD3+ CD4- CD8- phenotype). We obtained conflicting data about OK-NK and Leu 11 antibodies, which recognized CD16 antigen.
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PMID:[Cell morphology and surface markers in three patients with granular lymphocyte proliferative disorders of the T-cell type]. 810 90