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)

It can be difficult to differentiate the cells of infiltrating gliomas from macrophages associated with demyelinating lesions or cerebral infarcts, especially in tissue with freezing artifact or tissue that is technically suboptimal. We therefore sought to identify a reliable immunohistochemical marker for central nervous system macrophages that could be used on routinely processed tissue. The reactions of commercially available markers [Ham-56, Mac 387, CD68, CR3/43, DR alpha, lysozyme, CD16, and Ricinus communis agglutinin-1 (RCA-1)] were studied in normal cerebellum, subacute infarcts, viral encephalitis with microglial nodules, radiation necrosis, Alzheimer's disease, medulloblastoma, T-cell lymphoma, oligodendroglioma, gliomatosis cerebri, and microgliomatosis cerebri. We also performed a more extensive investigation of Ham-56 with largely surgical material. We concluded that (a) RCA-1 is a sensitive marker for microglia, either resting or responding to injury, but staining must be interpreted carefully because endothelial cells and reactive astrocytes frequently stain as well. This marker was useful in highlighting focal inflammation in HIV encephalitis. (b) CD68 is a specific marker for resting microglia. A case of microgliomatosis cerebri was intensely stained. (c) Ham-56 is a sensitive, specific (with the exception of endothelial cells), and reliable marker of central nervous system macrophages in routinely processed autopsy and surgical material. It is especially useful in distinguishing the macrophages in demyelinating disease and cerebral infarcts from neoplastic glial cells.
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PMID:Macrophage markers in diagnostic neuropathology. 137 20

A grave prognosis is usually associated with leukemic skin infiltrates (leukemia cutis). However, some leukemic skin infiltrates are clinically similar to reactive non-leukemic infiltrates in patients with leukemia; thus it is of great importance to distinguish them. Fifty-four cases which were thought clinically to be leukemia cutis underwent immunophenotyping with a panel of nine T, B, monocytic, and macrophage markers using paraffin sections. Immunohistochemistry helped identify 44 cases with leukemia cutis and 10 with reactive infiltrates. In all cases of leukemia cutis, the staining patterns of skin infiltrates were concordant with cell type in the bone marrow. Furthermore, the panel of markers was usually helpful in distinguishing reactive from leukemia infiltrates, especially in cases with chronic lymphatic leukemia. Immunohistochemistry is a valuable adjunct in histopathologic differentiation of skin infiltrates in most cases of leukemia. With formalin-fixed, paraffin-embedded biopsies, we recommend that CD45 (LCA), CD45RO (UCHL-1), CD3, CD20 (L-26), CD43 (Leu-22), CD68 (KP-1), lysozyme, and chloroacetate esterase be considered in cases of systemic leukemia with cutaneous papules and nodules that prove difficult to interpret with routine section.
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PMID:Value of immunohistochemistry in the diagnosis of leukemia cutis: study of 54 cases using paraffin-section markers. 138 98

To provide baseline information on the immunoarchitecture of normal bone marrow, we studied cryostat-cut, frozen, and paraffin-embedded, fixed tissue sections prepared from 21 core biopsies of normal bone marrow obtained during bone marrow harvests for transplantation. A large panel of antibodies was applied that included, for frozen tissue, Leu-6 (CD1), T11 (CD2), Leu-3a (CD4), Leu-1 (CD5), Leu-2a (CD8), J5 (CD10), My7 (CD13), Leu-11 (CD16), B4 (CD19), B1 (CD20), B2 (CD21), Tac (CD25), My9 (CD33), T200 (CD45), NKH-1 (CD56), kappa and lambda chains, beta F1, Ki-67, HLA-DR, TQ1, and keratin, and for fixed tissue, leukocyte common antigen (CD45), L26 (CD20), LN1 (CDw75), LN2 (CD74), LN3, LN4, LN5, MB1 (CD45R), MB2, MT1 (CD43), MT2 (CD45R), UCHL1 (CD45R0), BM1, Ki-1 (CD30), Leu-M1 (CD15), lysozyme, KP1 (CD68), actin, S100, neuron-specific enolase, vimentin, and keratin. On fresh-frozen sections CD19 and CD2 were the most reliable and sensitive markers for B and T cells, staining 5% and 9% of marrow cells, respectively. Immunoglobulins generally showed heavy background staining, which frequently precluded an accurate assessment. The CD4 to CD8 ratio in the bone marrow was reversed from that of peripheral blood. On fixed tissues, leukocyte common antigen was found in 14% of the marrow cells, corresponding roughly to the lymphocyte population. L26, a pan-B-cell marker, stained 3% of the marrow cells. Among the other B-cell markers, LN1 and MB2 stained a large number of cells (40% to 70%), indicating reactivity with cells of the myeloid or erythroid series in addition to lymphocytes. Among the T-cell markers, UCHL1 and MT1 stained 66% and 50% of the cells, respectively, which could be explained by their cross-reactivity with myeloid cells. Nonspecific myelomonocytic markers (Leu-M1, KP1, and lysozyme) also showed reactivity in a high percentage of cells. No particular architectural distribution patterns of B or T lymphocytes were noted in either frozen or fixed bone marrow specimens. The results of this study provide normal baseline data for the immunohistologic application of hematopoietic and lymphoid markers on frozen or fixed bone marrow biopsy specimens.
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PMID:Immunoarchitecture of normal human bone marrow: a study of frozen and fixed tissue sections. 159 93

Immunohistochemistry for the histiocyte antigens CD68, L1, factor XIIIa, and S100 protein was performed on 19 cases of angiomatoid malignant fibrous histiocytoma (MFH) and for keratin, leukocyte common antigen, factor VIII-related antigen, muramidase, and desmin on six of these cases. Nine of 19 cases expressed the histiocyte differentiation antigen CD68, and in three cases expression was seen in greater than 90% of cells. Of the 19 cases studied, three contained rare S100-positive tumor cells, and two expressed factor XIIIa within tumor cells. In three of the six cases, rare desmin-positive tumor cells were identified. The neoplastic cells did not express the other antigens studied. CD68 was not detected in any of 12 cases of storiform-pleomorphic and myxoid MFH or in any of 24 cases of normal tissues or nonfibrohistiocytic mesenchymal tumors except for granular cell tumors. These results indicate that either the cells of angiomatoid MFH differentiate along lines of a tissue macrophage or alternatively, and perhaps more likely, are mesenchymal tumors with a phenotypic alteration, paralleling an enhanced capacity for phagocytosis and acquisition of lysosomes. In either event, the immunophenotype contrasts with conventional MFH and provides another independent set of observations in support of a separation of angiomatoid from conventional MFH.
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PMID:Evaluation of CD68 and other histiocytic antigens in angiomatoid malignant fibrous histiocytoma. 131 23

The ultrastructural localization of the CD68 antigen, a 110-kd intracellular glycoprotein associated with myeloid cells and with monocytes/macrophages, was investigated in human neutrophil granulocytes by postembedding immunogold staining, using monoclonal antibody KP1. The antigen was found in the primary granules of neutrophils, although not all primary granules were labeled. It was absent from the plasma membrane. In monocytes, it was also detected within cytoplasmic granules, colocalized with lysozyme and myeloperoxidase. This observation confirms and completes results obtained by immunofluorescence and other light-microscopic methods. Moreover this study shows that the CD68 epitope recognized by antibody KP1 is able to resist fixation and embedment and therefore emphasizes the value of using KP1 as a marker for this macrophage-associated molecule.
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PMID:Ultrastructural localization of the CD68 macrophage-associated antigen in human blood neutrophils and monocytes. 171 19

Plexiform fibrohistiocytic tumour is a recently described, seemingly benign neoplasm of superficial soft tissue which is poorly recognized and the differentiation pattern of which remains obscure. Fourteen new cases are presented here. These presented predominantly in the upper limb of infants and children, although the age-range was wide. A morphological spectrum depending on the relative proportions of the spindle cellular and nodular histiocyte-like components was evident. Immunohistochemical analysis revealed positivity of tumour cells in both components for smooth muscle actin, suggestive of myofibroblastic differentiation, as was borne out ultrastructurally in two cases. In addition, a minority of the histiocyte-like cells were also CD68 positive but negative for leucocyte common antigen, HLA-DR, Mac387 and lysozyme. In view of the ultrastructural and other immunohistochemical results, this is regarded as further evidence that the CD68 epitope recognized by KP-1 is not confined to cells of monocyte/macrophage or myeloid lineage. Plexiform fibrohistiocytic tumour appears to be a clinicopathologically distinctive myofibroblastic neoplasm which may warrant reclassification in due course.
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PMID:Plexiform fibrohistiocytic tumour: clinicopathological, immunohistochemical and ultrastructural analysis in favour of a myofibroblastic lesion. 172 56

Immunologic studies have demonstrated that the vast majority of hematolymphoid neoplasms previously designated as "histiocytic" are lymphoid in origin. Consequently, malignancies of macrophage lineage are considered rare by most authors; indeed, their existence is doubted by some. Herein we report two cases of malignant histiocytic neoplasms (malignancies of macrophage lineage) of the small intestine. Both patients presented in the 7th decade with symptoms related to an abdominal mass. The polypoid tumors protruded into the intestinal lumen, extended through the entire thickness of the bowel wall, and involved regional lymph nodes. Microscopically, sheets of large pleomorphic histiocytic cells infiltrated around crypts and were associated with an admixture of bizarre giant cells and inflammatory cells. Mitotic figures were easily found. Ultrastructurally, the cells lacked desmosomes and had indented or kidney-shaped nuclei and cytoplasm containing mostly lysosomes and dense lipid droplets. In both cases, paraffin section immunohistochemistry revealed reactivity of tumor cells for CD45RB (LCA), CD45RO (A6), CD68 (KP1), CD15 (LeuM1), and lysozyme. Frozen section immunohistochemistry performed in one case further supported the macrophage phenotype. Southern blot studies of this case did not reveal immunoglobulin or T-cell receptor beta chain gene rearrangements. One patient initially treated by surgery only died of disease 3 years after diagnosis. The second patient is alive and disease-free 2 years following postoperative combination chemotherapy. The diagnosis of malignant histiocytic neoplasms requires the use of a panel of immunohistochemical markers and may be supported by electron-microscopic studies.
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PMID:Malignant histiocytic neoplasms of the small intestine. 172 94

The term "plasmacytoid T-zone cells" has been used to describe distinctive cells that occur in clusters in the paracortex of some reactive lymph nodes. Recently, tumorous proliferations of these cells have been described in several patients with myelomonocytic leukemias. Neither the nature of these cells nor their relationship to myeloid leukemia has been conclusively established. We report the case of a 64-year-old woman with chronic myelomonocytic leukemia who developed lymphadenopathy that proved to be due to tumorous accumulation of plasmacytoid T-zone cells in the interfollicular regions of the lymph nodes. She underwent splenectomy because of symptomatic splenomegaly; the resected spleen also contained aggregates of plasmacytoid T-zone cells, in addition to extramedullary hematopoiesis. On treatment with busulphan and prednisone, the lymphadenopathy resolved and did not recur. The patient died 7 years later with blast transformation of her myelomonocytic leukemia and no recurrence of lymphadenopathy. The aggregates of plasmacytoid T-zone cells were architecturally and cytologically distinct from the leukemic infiltrates of myeloid cells in the spleen, and there was no evidence of differentiation of these cells into myeloid or monocytic cells. A panel of monoclonal antibodies on paraffin sections revealed no lineage-specific T- or B-cell markers (UCHL1-, L26-), and the plasmacytoid cells were positive for CD68 (KP1) and L60 (CD43), as well as faintly positive for 4KB5 (CD45RA) and MB1 (CD45R). They did not stain with antibodies to myeloid lineage antigens CD15, lysozyme, or myeloperoxidase. The combination of clinical, morphologic, and immunologic features of plasmacytoid T-zone cells in this case suggests that these cells may be of monocytic lineage but are not direct precursors of mature monocytic or granulocytic cells, and may not be part of the neoplastic clone in patients with myelomonocytic leukemia.
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PMID:Plasmacytoid T-zone cell proliferation in a patient with chronic myelomonocytic leukemia. Histologic and immunohistologic characterization. 184 25

An immunophenotype was performed on an osteoclast-like giant cell tumor of the pancreas using a panel of antibodies to epithelial and leukocyte antigens. Several antibodies to cytokeratin and carcinoembryonic antigen were negative in the tumor. Osteoclast-like cells were positive for CD4, CD13, CD45, CD68, CD71, and vimentin, but negative for lysozyme and HLA-DR. Mononuclear tumor cells were positive for CD4, CD11c, CD13, CD14, CD45, CD68, CD71, HLA-DR, and vimentin, but negative for lysozyme. The phenotype is similar to that previously described for giant cell tumor of bone. The osteoclast-like cell phenotype is also similar to that reported for normal osteoclasts. The findings support a nonepithelial origin for osteoclast-like giant cell tumor of the pancreas, and suggest a derivation similar to giant cell tumor of bone.
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PMID:Osteoclast-like giant cell tumor of the pancreas: immunophenotypic similarity to giant cell tumor of bone. 186 95

The phenotype of inflammatory cells in lymph nodes from 16 patients with culture-proven tuberculous lymphadenitis were examined by histological and immunohistochemical techniques. Eight patients were suffering from a symptomatic HIV1 infection and 8 patients were immunocompetent individuals without positive HIV1 serology. In addition, the lymph nodes of 2 AIDS patients with Mycobacterium avium-intracellulare infection were examined using the same techniques. Characteristic granulomas with or without caseation were observed in the 8 immunocompetent and the 4 HIV1-infected patients with less marked lymphopenia of CD4+ peripheral blood lymphocytes (PBL). In lymph nodes from the other HIV1-infected patients with more severe depression of CD4+ PBL, no epithelioid cell formation was present; instead, foamy macrophages were found. The phenotype of the macrophages underwent progressive changes in parallel with the decreasing numbers of CD4+ PBL. Foamy macrophages in M. avium-intracellulare infection exhibited remarkable erythrophagocytotic activity and may represent an end-stage phenotype. They were positive for S100 protein and did not produce lysozyme or alpha-1-antichymotrypsin. They lost the antigen which was detected by monoclonal antibody Mac387 whereas positivity for HLA-DR, CD68 and KI-M8 was preserved. While many lymphocytes expressed CD25 (IL2 receptor) in cases with typical granulomas, there was no such CD25 expression in cases without epithelioid cell formation. Although granulomas have been produced in experimental animals independently of cell-mediated immune mechanisms, our results suggest that T-cell functions are necessary for epithelioid granuloma formation in human tuberculosis.
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PMID:In situ immunophenotype of macrophages and lymphocytes in granuloma formation of tuberculous lymphadenitis in HIV-infected and immunocompetent patients. 189 41


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