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)

Bispecific heteroconjugate antibodies can bind soluble protein Ag to APC and thereby enhance Ag presentation. We used such antibodies to bind hen egg lysozyme (HEL) to various structures on the surface of normal splenic B cells to determine which structures would provide the best targets for enhanced presentation. We found that HEL was presented efficiently to hybridoma T cells if bound to sIgD, sIgM, or class I or II MHC molecules, but not at all if bound to Fc gamma RII, or B220 molecules on B cells. The efficiency of presentation of HEL was measured as a function of the amount of 125I-HEL bound per cell. HEL was presented with 5 to 10 times greater efficiency when bound to sIg, than when bound to MHC molecules. When compared on the basis of the amount of HEL bound, sIgD and sIgM functioned equally as target structures, as did class I and class II MHC molecules. Large amounts of HEL bound to B220, but no presentation resulted, indicating that focusing HEL to the APC surface was not sufficient for presentation to occur. HEL was internalized rapidly and in large amounts when bound to sIgD or sIgM, but slowly and in small amounts, when bound to class I or class II MHC molecules. Thus, a rapid rate of internalization may in part explain the high efficiency of Ag presentation after binding to sIg. However, the small amount of HEL internalized via MHC molecules was utilized efficiently for presentation. These results indicate that sIgM and sIgD serve equally on normal B cells to focus and internalize Ag and enhance Ag presentation, but that class I or class II MHC molecules can also be used to internalize Ag and enhance Ag presentation, perhaps by a separate intracellular processing pathway.
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PMID:Efficiency of antigen presentation after antigen targeting to surface IgD, IgM, MHC, Fc gamma RII, and B220 molecules on murine splenic B cells. 247 43

Extramedullary tissue infiltrates of acute myeloid leukemia are rare and often difficult to recognize in routine paraffin-embedded tissue sections. Since appropriate therapy for these tumors depends on their precise identification, we have studied a series of tissues infiltrated with primitive myeloid cells using monoclonal and polyclonal antibodies capable of labeling cells of the myeloid/monocytic system in paraffin-embedded tissue sections. The current retrospective study involved tissues from 15 patients (eight men and seven women) with a mean age of 51 years (range, 23-77). A diagnosis of extramedullary myeloid cell tumors had been made on the basis of routine histology, chloroacetate esterase cytochemical stain, and--in some cases--electron microscopy. Paraffin-embedded tissue sections were cut and stained employing the alkaline phosphatase antialkaline phosphatase (APAAP) immunocytochemical procedure with monoclonal antibodies against leukocyte-common antigen (PD7/26-2B11), restricted components of the leukocyte-common antigen (UCHL1, 4KB5), granulocytes (Mac-387, Leu-M1), leukocytes (MT1, MT2, LN1, LN2), HLA-DR (LN3), and elastase (NP57), as well as polyclonal antibodies against lactoferrin, lysozyme, alpha-1-antitrypsin, and alpha-1-antichymotrypsin. Results indicate that antibodies against Mac-387, elastase, and lysozyme are most useful in the recognition of neoplastic myeloid cells. We conclude that tissues containing granulocytic tumors can be identified in paraffin-embedded tissue sections using a panel of antibodies and the APAAP procedure.
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PMID:The immunophenotyping of extramedullary myeloid cell tumors in paraffin-embedded tissue sections. 297 Aug 8

Reagents that recognize antigens on lymphoid cells in fixed and wax-embedded sections have been applied to a series of cases of non-Hodgkin's lymphomas. The panel consisted of MB1, 4KB5 (CD45r), LN1, L26 and MB2 which recognize antigens expressed predominantly on B-lymphocytes; UCHL1 and MT1 which recognize antigens expressed on T-lymphocytes and myeloid cells; antibodies recognizing the non-lineage antigens LeuM1 (CD15), BerH2 (CD30), anti-EMA; anti-lysozyme and MAC 387 which detect antigens present on some macrophages; and finally TAL1B5 (class II MHC), CAM 5.2 (low molecular weight cytokeratin) and PD7/26 + 2B11(CD45). Two hundred and four cases of non-Hodgkin's lymphoma have been studied, of which 158 had been fully characterized on frozen sections. The series was biased towards high-grade (n = 108) and T-cell (n = 44) tumours and these were largely prospectively accrued. It was found that discrimination between B-cell and T-cell lymphomas can be reliably achieved using these reagents and that a small panel (CD45, L26, MB2, MT1, UCHL1) is adequate for this purpose. Using the full range of reagents it is not possible to subdivide cases into groups that correspond with morphological subtypes of lymphoma. Although paraffin section immunohistochemistry is of value, the diagnosis of lymphoproliferative disorders must still be based upon the assessment of well fixed, carefully prepared tissue sections using conventional tinctorial methods.
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PMID:Paraffin section immunohistochemistry. I. Non-Hodgkin's lymphoma. 326 64

Mammary ductal foam cells are present in normal breast tissue as well as in a number of breast diseases. Such foam cells tend to be in particular abundance with fibrocystic changes of the breast. Foam cells may appear within duct lumens or plastered in cohesive masses along duct walls, simulating an epithelial structure. The nature and origin of these innocuous-appearing cells, based on morphologic studies, remain a controversy, for they appear to be of epithelial derivation. This study was undertaken to determine the nature of intraductal "foam" cells and their origin in the breast. Nine cases of adult fibrocystic disease were examined immunohistochemically with antibodies to cytokeratins (Mak-6, Cam 5.2), leukocyte common antigen, and the following macrophage antibodies: KP-1 (CD68), HAM 56, and MAC 387. The lysozyme and alpha-1-antitrypsin content of foam cells also was studied. The immunohistochemical data in this study confirm the macrophage character of these foam cells, which are positive for CD68, HAM 56, and MAC 387, lysozyme, and alpha-1-antitrypsin and negative for leukocyte-common antigen and cytokeratins.
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PMID:Mammary ductal foam cells: macrophage immunophenotype. 811 24

An immunohistochemical study by avidin-biotin-peroxidase was performed on paraffin-embedded and decalcified bone marrow biopsies in 31 acute leukemias (19 myeloid and 12 lymphoblastic). The Ulex Europaeus lectin and 14 antibodies (anti-CD45, -CD34, -myeloperoxidase, -lysozyme, -CD15, -CD68, -carcinoembryonic antigen, -factor VIII-related antigen, BNH9, anti-CD45RO, -CD3, -CD20, DBB42 and DBA44) were tested. All acute myeloid leukemias from M0 to M5 type were stained by either the anti-myeloperoxidase or anti-lysozyme antibodies. CD68, CD15 and the carcinoembryonic antigen were respectively expressed in 80%, 40% and 20% of myeloid leukemias from M1 to M5 type. The Ulex Europaeus lectin and the anti-factor VIII-related antigen antibody stained only the M7 leukemia and the anti-CD3 antibody stained only the T acute lymphoblastic leukemia. DBB42 was expressed by 63% of B-lineage lymphoblastic leukemias and CD20 by 36%. No leukemia was stained by DBA44. Immunohistochemistry on bone marrow biopsy can assess the lineage of most acute leukemias with the use of a panel of antibodies such as the anti-myeloperoxidase, -lysozyme, -CD68, -CD20, DBB42, -CD3, BNH9, anti-factor VIII-related antigen antibodies and the Ulex Europaeus lectin.
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PMID:[Immunohistochemical characterization of acute leukemia. Study of 31 bone marrow biopsies]. 753 64

The diagnosis of primitive hematologic malignancies in extramedullary sites (lymphoblastic lymphoma of T- or B-cell type and myeloid sarcoma) on paraffin-embedded tissue sections is difficult and often impossible because of the primitive morphology of the neoplastic cells. The authors studied 21 extramedullary tumors of lymphoid or myeloid blasts. They used a panel of 22 antibodies on frozen sections and 9 antibodies on paraffin sections to determine the spectrum of immunophenotypes and to develop a practical panel for diagnosis. All but two of the cases could be classified as lymphoid or myeloid using immunohistologic analysis. Thirteen cases were classified as lymphoblastic lymphoma/acute lymphoblastic leukemia (LBL/ALL); 10 were classified as precursor T (CD7+, CD3+/-, CD45+) and 3 as precursor B-cell (CD19+/-CD10+CD45-) type. Five cases were classified as myeloid sarcoma (CD13+ myeloperoxidase+, lysozyme+). Two LBL/ALL coexpressed either CD33 (1 case) or CD15 (1 case), and one myeloid sarcoma coexpressed TdT and CD7. One case appeared to be truly mixed lineage, coexpressing CD3 with myeloperoxidase and lysozyme, and two cases expressed no lineage-specific antigens. There were clinical differences between the three major tumor types, and within the category of T-precursor LBL/ALL, classification according to stage of thymocyte differentiation was associated with distinctive clinical features. In conclusion, the spectrum of immunophenotypes detected on frozen section was similar to that reported by flow cytometry on peripheral blood and bone marrow specimens. The most useful antigens on frozen sections were CD7 and CD3 (T cell), CD10 and CD19 (B cell), and CD13 (myeloid). TdT was coexpressed by one myeloid sarcoma and was undetectable in 40% of LBL/ALL. On paraffin sections, myeloperoxidase and lysozyme were reliable markers of myeloid lineage, but none of the markers used on paraffin sections distinguished between LBL/ALL of T- and B-precursor types. Both B-LBL/ALL and myeloid sarcomas were often CD45- on paraffin sections, which may be a obstacle in determining the diagnosis. These distinctions appear to have clinical relevance.
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PMID:Extramedullary tumors of lymphoid or myeloid blasts. The role of immunohistology in diagnosis and classification. 757 94

Regulation of B lymphocyte development by the mu-membrane (mu m) and delta-membrane (delta m) heavy chains of Ig was examined in an Ig transgenic mouse model. Mice were bred on a common C57BL/6 (B6) background, and expressed rearranged and hypermutated heavy and light chain transgenes encoding high-affinity receptors for the foreign antigen hen egg lysozyme (HEL). At no stage were they exposed to HEL. Variation of the Ig heavy chain construct yielded four different types of Ig transgenic mice in which developing B lineage cells either expressed mu m and delta m in the normal physiological sequence (mu m then mu m + delta m), or produced mu m alone, delta m alone or mu m + delta m from the onset of heavy chain expression in the bone marrow. Immature B220low, HSAhigh and mature B220high, HSAlow B cells were produced in all mice regardless of their developmental pattern of mu m and delta m expression. However, production of immature B cells was most efficient when mu m heavy chain was expressed alone during early B cell development. Thus expression of delta m during this period either in the presence or absence of mu m resulted in a 2- to 3-fold reduction in the numbers of immature B cells in the spleen as well as altered levels of surface B220 and HSA on these cells in spleen and bone marrow respectively. By contrast, normal maturationally regulated expression of delta m led to the presence of increased numbers of mature B cells in the spleen and lengthened the average lifespan of these cells as determined by in vivo incorporation of 5-bromo-2'-deoxyuridine. These results pointed to selective effects of mu m and delta m heavy chains on regulation of the early and late stages of B cell development respectively, and provided a rational basis for co-expression of mu m and delta m as well as the delayed expression of delta m during normal B cell development.
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PMID:Differential regulation of early and late stages of B lymphocyte development by the mu and delta membrane heavy chains of Ig. 769 8

BCG infection of mice provides a convenient model to study natural and cellular immunity to mycobacteria and the mechanisms of granuloma formation and repair. We have used a range of macrophage (M phi) membrane molecules and secretory products to investigate resident M phi-pathogen interactions and T lymphocyte-dependent recruitment and activation of M phi in different tissues of immature, normal adult and gamma interferon deficient animals. In situ hybridization (ISH), RT-PCR and immunocytochemical analysis of M phi gene and product expression have been correlated with in vitro study of endocytic and secretory activity in which biogel polyacrylamide bead-elicited peritoneal M phi are exposed to Th1 and Th2 cytokines, LPS, BCG and other stimuli. The role of resident and newly recruited M phi responding to BCG in liver, spleen, lung and brain has been defined by means of antigen markers expressed by M phi (F4/80, 7/4, CR3, macrosialin, sialoadhesin and scavenger receptor) and/or T and B lymphoid cells (MHC Class II, CD4, CD8, B220). Heterogeneity in M phi secretory activity was revealed by ISH analysis of lysozyme, TNF-alpha, IL-1 IL-6 and MCP-1, by in vitro assay of NO and superoxide anion production, and by RT-PCR studies of Th1 (interferon gamma) and Th2 (IL-4, IL-13, IL-10) lymphokine mRNA in tissues. Our studies confirm the importance of interferon gamma as a critical mediator of host resistance to mycobacterial infection and raise intriguing questions in regard to T cell and M phi functional heterogeneity in distinct tissue microenvironments.
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PMID:BCG-induced granuloma formation in murine tissues. 771 50

In evaluating histologically malignant infiltrates in the skin, it is often challenging to distinguish granulocytic sarcoma (GS) from selected cases of peripheral T-cell lymphoma (PTCL). These lesions have clinical features in common, in addition to shared histologic attributes. These include similarity in dermal distribution and growth pattern, nuclear characteristics, propensity to recruit other inflammatory cell types, and production of matrical sclerosis. In order to determine if immunohistology could contribute to differential diagnosis in this setting, we analyzed 15 cases of mucocutaneous GS, and compared them with 11 cases of well-documented PTCL. Antibodies in the CD15, CD20, CD34, CD43, CD45, CD45RO, and CD68 groups were used, as well as anti-myeloperoxidase (anti-MPX), anti-lysozyme (anti-LYSO), Mac387, and MB2. Anti-LYSO and anti-MPX were sensitive and specific markers of GS, labeling 93% and 80% of GS cases, respectively, and no cases of PTCL. Anti-CD15 and MB2 were also specific for GS, but each labeled only 60% of GS cases. CD34, CD68, and Mac 387 were specific but insensitive markers of GS. CD43 and CD45 were not particularly useful discriminants, with each being seen in 93% of GS cases, but also 64% and 100% of cases of PTCL, respectively. CD45RO was specific for PTCL; it was present in 82% of PTCL cases and no GS cases. Thus, conjoint reactivity for CD43, CD45, MPX, and LYSO characterizes GS, and differs from the pattern of PTCL, which is characterized by reactivity for CD45 and CD45RO, occasional reactivity for CD43, and lack of other specified markers.
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PMID:Granulocytic sarcoma: an immunohistologic comparison with peripheral T-cell lymphoma in paraffin sections. 796 23

Two cases with primary gastric Ki-1 positive anaplastic large cell lymphoma are presented. Morphologic features of both cases involved pleomorphism of the neoplastic cells, fibrosis and lymphatic infiltration. The neoplastic cells in both cases were positive for BerH2 (CD30), LCA(CD45), lysozyme and alpha-1-antitrypsin (alpha 1-AT). In additional case, the neoplastic cells were additionally positive for MAC387 and alpha 1-antichymotrypsin (alpha 1-ACT). The neoplastic cells in these cases were negative for L26(CD20), UCHL-1(CD45RO), DAKO CD3 and epithelial membrane antigen (EMA). According to the results of the phenotypic studies, the authors consider that the neoplastic cells have some of the features of histiocytes. Both patients at 2 and 8 years after surgery without chemotherapy are disease free. This lymphoma is well known to be frequently misdiagnosed as undifferentiated carcinoma. Although rare in occurrence, recognition of this primary lymphoma in the stomach has a significant clinical implication, as the authors consider that its prognosis might be better than undifferentiated carcinoma of the stomach.
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PMID:Primary gastric Ki-1 positive anaplastic large cell lymphoma: a report of two cases. 802 56


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