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:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gut associated lymphoid tissue in 15 normal appendices has been characterised in tissue sections using both morphological criteria and immunocytochemical techniques. A panel of monoclonal and polyclonal antibodies was used including antibodies to B-cells, T-cells, macrophages, HLA DR and immunoglobulins. The lymphoid tissue in the appendix was shown to bear a strong resemblance to that in lymph nodes with the exception of the region where the appendix follicles associate with the dome epithelium, which has no lymph node equivalent. This zone of cells between the lymphoid follicles and the dome epithelium termed the 'mixed cell zone' has been shown to contain an abundance of HLA DR-bearing cells, some of which have irregular nuclear morphology and resemble follicle centre cells. These cells were seen to extend into the epithelium of the dome but not the crypts. Using a monoclonal anti-B-cell antibody a population of B-cells was detected in the equivalent areas of mixed cell zone and epithelium and quantitative studies showed that these intraepithelial B-cells comprised approximately 4-5% of the cells in the epithelium. The mixed cell zone was also seen to contain T-cells, S-100 protein-containing macrophages and occasional lysozyme-containing macrophages. Plasma cells were rarely seen in this area.
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PMID:Gut associated lymphoid tissue: a morphological and immunocytochemical study of the human appendix. 387 11

Immunoperoxidase study can be performed either on fixed and paraffin embedded biopsy specimens or on frozen sections. Advantages and limits of these two methods, as well as the results obtained on normal and pathologic lymphoid tissue are presented. Immunoperoxidase on paraffin sections (PAP technic) is a simple method which allows a good morphologic analysis. However, most of the fixatives destroy proteic antigens particularly those linked to the cell membrane. Thus surface immunoglobulins (S.Ig) cannot be detected. In contrast cytoplasmic immunoglobulins remain antigenic enough to be demonstrated in routine paraffin embedded sections. In lymphomas synthesizing monotypic immunoglobulins, the percentage of labelled cells varies from 5 to 80%. Beside the background staining, which can be attenuated by trypsinisation, absorption of extracellular substances is often responsible for a false positive staining. Pathologists are mainly confronted with the passive uptake of extracellular immunoglobulins (IgG K and IgG L), as well as other serum proteins (lysozyme etc...). Immunoperoxidase on frozen sections allows the use of monoclonal antibodies. A large number of surface and cytoplasmic antigens can be detected. First, the localization of B and T lymphocytes, NK cells, interdigitating cells and dendritic reticulum cells within the normal lymph node is described. In the second part, the interest of monoclonal antibodies in differential diagnosis between lymphoma and pseudo-lymphoma, and in phenotyping of lymphomas is discussed. Now, it is possible to perform an in situ immunologic characterization of most lymphomas. B cell lymphomas have sIg associated with other antigens (Pan B+, HLA-DR+). Cells of chronic lymphoid leukaemia and centrocytic (cleaved-cell) lymphomas frequently express T65 (T 101+ or Leu 1+) antigen which is usually found on normal or neoplastic T lymphocytes. Monoclonal antibodies provide new evidence of the germinal centre origin of follicular lymphomas. Thus, monoclonal antibody directed against dentritic reticulum cells (CRD) revealed the same network of DRC in follicular lymphomas as in reactive germinal centres. This finding could account for the nodular pattern of these lymphomas, neoplastic cells being in some way, enclosed within the DRC network. On the other hand, neoplastic follicles are surrounded by a large amount of t lymphocytes. Some T lymphocytes are also found within the follicles where they are associated with NK cells. Lastly, as reactive benign follicles, neoplastic follicles are labelled by the anti-Calla antibody.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Immunoperoxidase study of normal and pathologic lymphoid tissue. Value of monoclonal antibodies]. 638 12

Surface marker analysis with rosette tests and a large panel of xenoantisera and monoclonal antibodies was done on the malignant cells of 55 patients with acute myeloid leukemia (AML). The diagnosis was made on morphological and cytochemical grounds, and the leukemias were classified according to the quantified FAB criteria. The marker tests included the E- and EA-rosette test, immunofluorescence with rabbit-polyclonal antisera against human Ig, kappa, and lambda light chains, thymocytes, granulocytes, erythrocytes, platelets, lysozyme, (leukemic) myeloblasts, the common ALL antigen, SB cell-line cells (anti-Ia), and a mouse anti-Ia serum. The monoclonal mouse antibodies applied were anti-T-cell antibody (3A1), two anti-granulocyte-monocyte antibodies (OKM1 and B2.12), four antigranulocyte antibodies (MI/N1, UJ 308, B4.3, and B13.9), an antiplatelet antibody (C17.28), anti-HLA heavy chains (w6/32.HLK), anti-Ia antigen (OKI1), and OKT10. AML cells from many patients lacked the expression of myeloid markers, and we found that a correlation existed between the relative maturity of the leukemia subtype and the extent of positivity for these markers. Surface marker analysis discriminated poorly between the "myeloid" and "monocytoid" subtypes; OKT10 and the "T-cell marker" 3A1 were often expressed on AML cells. In two cases of AML, there was an unexpected expression of platelet antigens with the monoclonal antiplatelet antibody. One of them, classified as M1, was ultrastructurally a megakaryoblastic proliferation with a positive reaction for platelet peroxidase. Only with the help of computerized analysis, was it possible to prove a clear correlation between the surface marker profile and the FAB classification.
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PMID:A comparison of surface marker analysis and FAB classification in acute myeloid leukemia. 657 76

A human leukemic cell line (THP-1) cultured from the blood of a boy with acute monocytic leukemia is described. This cell line had Fc and C3b receptors, but no surface or cytoplasmic immunoglobulins. HLA haplotypes of THP-1 were HLA-A2, -A9, -B5, -DRW1 and -DRW2. The monocytic nature of the cell line was characterized by: (1) the presence of alpha-naphthyl butyrate esterase activities which could be inhibited by NaF; (2) lysozyme production; (3) the phagocytosis of latex particles and sensitized sheep erythrocytes; and (4) the ability to restore T-lymphocyte response to Con A. The cells did not possess Epstein-Barr virus-associated nuclear antigen. These results indicate that THP-1 is a leukemia cell line with distinct monocytic markers. During culture, THP-1 maintained these monocytic characteristics for over 14 months.
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PMID:Establishment and characterization of a human acute monocytic leukemia cell line (THP-1). 697 Jul 27

Although several attempts at the immunohistochemical characterization of histiocytosis have recently been made there is only one paper which reports a case of cerebral Langerhans cell histiocytosis (LCH) diagnosed by biopsy. This paper presents a bioptically diagnosed case of juvenile histiocytosis. The panel of antibodies used was as follows: anti-S-100, 2 different antibodies to anti-interleukin 2, anti-lysozyme, anti-LEU M1, anti-MAC 387, anti-major histocompatibility complex II and anti-GFAP. Microglia markers--Griffonia simplicifolia and RCA 1 lectins were also utilized. The proliferating cells produced a positive response to S-100, lysozyme and a partially positive response to HLA DR, but responded negatively to MAC 387, LEU M1, lectins, IL2R and GFAP. Our results were compared and analyzed in the light of those obtained by other authors.
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PMID:Immunohistological study of a case of cerebral Langerhans cell histiocytosis in brain biopsy. 772 76

The asialoglycoprotein (ASGP) receptor undergoes constitutive endocytosis in HepG2 cells, which is regulated by tyrosine kinase activity (Fallon, R. J., Danaher, M., Saylors, R. L., and Saxena, A. (1994) J. Biol. Chem. 269, 11011-11017). In this study we show that the receptor copurifies with a tyrosine kinase activity, as defined by tyrosine phosphorylation of an exogenous substrate (reduced carboxyamidomethylated and maleylated lysozyme). Analysis of cells transfected with one subunit of the ASGP receptor showed that signals in the cytoplasmic domain of the H1 subunit are sufficient for receptor kinase association. In addition, receptor kinase association is not dependent on the single cytoplasmic tyrosine at position 5. Analysis of the components of anti-ASGP receptor immunoprecipitates revealed the presence of a 127-kDa protein (p127), which becomes phosphorylated on tyrosine upon addition of gamma-[32P]ATP and which is capable of binding ATP.p127 was also demonstrated in anti-transferrin receptor immunoprecipitates but not in immunoprecipitates of a resident membrane protein, human HLA. In conclusion, these data demonstrate that the ASGP receptor, a protein that participates in constitutive, rapid endocytosis, is associated with a cellular tyrosine kinase.
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PMID:The asialoglycoprotein receptor is associated with a tyrosine kinase in HepG2 cells. 792 94

The behavior of mouse I-Ak molecules was studied in the human Ag presentation mutants T2 and 9.5.3, which contain deleted or mutated HLA DM genes. HLA class II molecules expressed by these APC are defective in presentation of native Ag and are mostly complexed with class II-associated invariant chain peptides (CLIP). In contrast to human class II molecules, a significant proportion of mouse I-Ak molecules expressed in T2 and 9.5.3 were associated with antigenic peptides, indicating that I-Ak/peptide assembly is possible in the absence of the Dm proteins. Thus, the presentation of determinants derived from hen egg lysozyme (HEL), keyhole limpet hemocyanin, and conalbumin was normal in 9.5.3Ak and a conalbumin determinant was presented normally by T2.Ak. However, the keyhole limpet hemocyanin determinant was not presented by T2.Ak, and HEL46-61 was only presented at a low level by these APC. SDS-stable, dimeric I-Ak molecules were expressed by both T2.Ak and 9.5.3Ak and formed late in their intracellular transport. Presentation of HEL46-61 was partially inhibited by disrupting vacuolar acidification in 9.5.3Ak, consistent with I-Ak/peptide assembly in a post-Golgi endosomal compartment. Accordingly, Dm is not an obligatory requirement for MHC class II/peptide assembly. We propose that Dm influences the displacement of CLIP from recently synthesized class II molecules, a process that is likely to be less critical for I-Ak because of its low affinity for CLIP.
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PMID:Antigen presentation and assembly by mouse I-Ak class II molecules in human APC containing deleted or mutated HLA DM genes. 798 44

Thirteen dermal cylindromas (DC) have been studied immunohistochemically using a panel of antibodies that stain different portions of normal eccrine and apocrine glands. Distinct staining patterns were found in the different cell populations of the tumor. Although the expression of cytokeratins (CK) 19 and 1/10/11 in occasional duct structures could indicate excretory (ductal) differentiation, a link between DC and apocrine secretory coil is suggested by the expression of alpha-1-antichymotrypsin, lysozyme, human milk factor globulin 1, alpha smooth muscle actin (1A4), and CK 8 and 18. The presence of intermingled S-100 protein-, HLA DR-, and CD1a-positive cells argues for the existence of Langerhans cells within the neoplasm. DC shares epithelial membrane antigen, carcinoembryonic antigen, mucin-like carcinoma-associated antigen (B12), laminin, collagen IV, fibronectin, and CD34(QBEND/10) expression with both eccrine and apocrine glands.
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PMID:Dermal cylindroma. An immunohistochemical study of thirteen cases. 859 35

The FACS-analysis of diseases as different as cancer, autoimmune disorders and chronic (retro)viral infections, including HIV-infection, shows -at least temporarily- a common feature of lymphocyte hyperactivation, characterized by cellular activation markers (HLA-DR, CD26, CD38, CD69, CD2R and/or CD30), as well as by solubilized membrane structures, such as beta-2m, sICAM-I, sIL-2R/sCD25, sCD8, and by some oversecreted immunocyte products (e.g. neopterin, lysozyme and/or cathepsin D). We tested two potential approaches to down-regulate the pathologically elevated CD8+ and HLA-DR+ T cells: (a) In animal model, we tested the sensibility of these, disease inducing and maintaining T cell subsets to in vitro pretreated (cell death preprogrammed) semi-syngeneic and allogeneic donor T cells in tumor-bearing mice. (b) In the first clinical study, we used a novel combination of FDA-approved drugs which inhibits Ca(2+)-influx and concomitantly down-regulates cytosolic cAMP in patient's overstimulated immunocompetent cells. We could achieve a 94.6-100% long-term survival in tumor-bearing mice. In patients, large primary tumors and large metastases shrinked by 80-85% and small metastases disappeared completely. Since in HIV-infected persons, the increased number of HLA-DR+ CD38+T (T8) cells is associated with a fall in CD4-level and with development of AIDS, we are looking for the elimination of these HLA-DR+ targets by our novel technique in two AIDS-simulating (FIV/FeLV and SIV) animal models.
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PMID:Treatment of solid tumors should obligatorily be combined with the in vivo codepletion of tumor-protecting, CD8+/HLA-DR(+)-suppressor T cells by alloreactive donor T cells whose preprogrammed cell death allows a high GvL-effect before GvHD can be established. Results of animal experiments, including more than 6000 mice. 873 48

The disulfide reduction kinetics in equine lysozyme (ELZ), which is a Ca(2+)-binding lysozyme, and human (HLA) and equine alpha-lactalbumin (ELA) at pH 8.5 and 25 degrees C by excess dithiothreitol were studied, and it was found that in ELZ there is no superreactive disulfide bond, while one of the disulfides is reduced very quickly by the reducing agent in HLA and ELA, as in bovine alpha-lactalbumin. The local conformation around the surface disulfide in ELZ seems to be more similar to that in hen egg-white lysozyme than in alpha-lactalbumin. The four disulfides in ELZ were reduced slowly in an apparently single-exponential form, and the bound Ca2+ lowered the reduction rate. The torsion energy on each of the disulfides in three alpha-lactalbumin and eight c-type lysozymes whose native conformations have been experimentally or theoretically analyzed was calculated, and it was found that torsion imposed on the surface disulfide between Cys 6 and Cys 120 in alpha-lactalbumin is a main cause of the superreactivity and all of lysozymes, including the Ca(2+)-binding ones, have no such strained surface bond.
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PMID:The superreactive disulfide bonds in alpha-lactalbumin and lysozyme. 874 34


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