Macroglobulinemic neuropathy. Experimental macroglobulinemic neuropathy in mice.
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Biomedical subjects
S M Baird
Publications and source records attributed to S M Baird.
Amplification of the murine leukemia virus Mr 70,000 glycoprotein gene product by human xenografts in athymic mice.
Passage of human tumors in athymic mice is accompanied by an increase in serum levels of the Mr 70,000 murine leukemia virus envelope protein, gp70. Elevated levels of gp70 can be detected in tissues of the hematopoietic systems of mice bearing human xenografts, but there is no evidence of synthesis of gp70 in these tissues. By far, the highest concentration of gp70 is in the human xenografts themselves. When assayed for gp70, 8 human xenografts and 12 cell lines established from human xenografts were all positive. In the plasma membrane of the human astrocytoma xenograft, T24, the gp70 was found to be approximately 10% of the total membrane protein. In contrast, the concentration of the Mr 30,000 viral core protein, p30, was 17-fold less. Only trace amounts of complete infectious virus could be detected. A human prostate carcinoma line that had not been grown in the athymic mice was found to have no gp70, but was shown to be able to synthesize gp70 after a single passage in the athymic mice.
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Altered cell surface antigen expression in bladder carcinoma detected by a new hemagglutinating monoclonal antibody.
A hemagglutinating monoclonal IgM antibody (MoAb145) was produced against a high incidence red blood cell membrane antigen. By the specific red cell adherence test, the antibody also reacted with human bladder epithelium; in addition, expression of the MoAb145 antigen was lost in some cases of transitional cell carcinoma of the bladder, in a manner similar to the ABH blood group. Hemagglutination studies with a panel of erythrocytes lacking specific high incidence red blood cell membrane antigens indicated that MoAb145 did not recognize ABH specificity but rather a determinant absent from rare MN variant erythrocytes, including En(a-) erythrocytes, which lack glycophorin-alpha. Failure of MoAb145 to stain, by indirect immunofluorescence, the erythroleukemia cell line K562, which expresses glycophorin-alpha and the MN blood group, and failure to inhibit MoAb145 hemagglutination with an erythrocyte sialoglycoprotein fraction that contained MN blood group activity suggests that MoAb145 does not recognize either glycophorin-alpha or the MN blood group, but rather another membrane determinant, which is altered in En(a-) erythrocytes. This study demonstrates a new epitope detected by MoAb145 that is shared between human erythrocyte membranes and bladder epithelia, and is affected by neoplastic transformation in transitional cell carcinoma of the bladder.
ABO Blood-Group System↗
Murine T-lymphoma 'immunoglobulin' is identical to leukemia virus gp 70.
We have used chicken anti-mouse immunoglobulin antiserum to precipitate molecules from mouse T-lymphoma cells that had been radioiodinated. We analysed the immunoprecipitates by two-dimensional gel electrophoresis and compared the results with immunoprecipitates generated by other antisera. We found that the molecule precipitated by chicken anti-mouse immunoglobulin from T-lymphoma cells was identical to the mouse leukemia virus envelope glycoprotein (gp 70) produced by the T-lymphoma. Mouse IgM myeloma proteins block precipitation of T-lymphoma molecules by chicken anti-mouse immunoglobulin. We conclude that mouse IgM and gp 70 share antigenic determinants. This may lead to erroneous conclusions about the presence of immunoglobulin on T-cells.
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Membrane antigen on Epstein--Barr virus-infected human B cells recognized by a monoclonal antibody.
This paper describes a monoclonal antibody (B532) that detects a membrane antigen present on greater than or equal to 95% of the B cells from lines carrying the Epstein-Barr virus (EBV) genome. Evidence suggesting that B532 is EBV-related was originally obtained by using a cell-binding radioassay with different cell line substrates. Immunofluorescence and cell-sorter analysis confirmed that the antigen was present in high density on all EBV-infected lymphoblastoid B-cell lines, but not on EBV-negative B-, T-, myeloid, or null cell lines. Isolated normal peripheral blood B and T lymphocytes and monocytes failed to bind B532. The monoclonal antibody did not inhibit in vitro EVB infection nor did it block the killing of EBV-infected targets by cytotoxic T lymphocytes. The cell surface antigen recognized by B532 was shown by immunoprecipitation to have a molecular weight of approximately 45,000.
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Induction of sarcomas in athymic mice.
During the course of serial passage of 50 human xenografts in the athymic mouse over a period of 5 years we have observed two cases of induction of sarcomas in the murine stromal tissue associated with the human xenografts. Both times the growth of the murine sarcomas overtook that of the human xenograft. This change was monitored by analysis of the lactate dehydrogenase isozyme profile and histology of each passage of the human xenografts in the athymic mice. The two murine sarcomas were subsequently established in tissue culture. The sarcoma cell lines were found to be malignant by morphological and growth characteristics and were tumorigenic. They contained large amounts of murine leukemia virus when assayed for reverse transcriptase activity by infection of mouse SC-1 cells and BALB/c and NIH Swiss fibroblasts with filtered supernates, and some type C virus particles were observed by electron microscopy in tumor tissues. However, we were unable to demonstrate the presence of murine sarcoma virus by in vitro transformation of fibroblasts or sarcoma formation in vivo will cell free filtrates. Preliminary biochemical data indicate that the sarcomas are extremely high in plasma membrane ATP phosphohydrolase.
Adenosine Triphosphatases↗
Induction of lymphoma in antigenically stimulated athymic mice.
Athymic mice infected with pinworms or carrying human tumor xenografts frequently develop a lymphoproliferative disorder which eventually leads to lymphoma. By immunofluorescent analysis of involved tissues, the lymphomas appear to be mixtures of null cells, B-cells, and T-cells. When each lymphoma is established in tissue culture, a predominant cell type grows out. We have now established lymphoma lines of null cells, B-cells, and T-cells. Lymphoma development is preceded by the secretion into the bloodstream of large amounts of murine leukemia virus M.W. 70,000 glycoprotein antigen; however, very little virus is produced. In vivo, the expression of viral envelope antigen appears within a few days after human tumor transplantation and precedes the development of lymphoma by about a month. Cells expressing viral antigens are first seen in the diffuse cortex of lymph nodes and the periarteriolar white sheath of the spleen, the tissue domains in which lymphomas also first appear.
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Induction of T- and B-lymphocyte responses in antigenically stimulated athymic mice.
Antigenic stimulation of athymic mice on the BALB/c background by infection with the pinworms Aspiculuris tetraptera and Syphacia obvelata or by xenografts of human tumors induced a proliferation of T- and B-lymphocytes in spleen and lymph nodes and occasional germinal center formation. The proliferating T-lymphocytes showed greater fluorescence per cell than the Thy 1-positive cells from unstimulated athymic mice when examined by cytofluorography using anti-Thy 1 antiserum. The proliferating T-lymphocytes were shown to be functional by their ability to help mount an in vivo antibody response to sheep erythrocytes and other thymus-dependent antigens. Spleen cells cultures taken from mice at early stages of antigenic stimulation responded in vitro to the thymus-dependent mitogens concanavalin A and phytohemagglutinin. However, spleen cell cultures taken from mice chronically stimulated by foreign antigens were apparently already maximally stimulated and showed no further stimulation when incubated with concanavalin A or phytohemagglutinin in vitro.
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Human T cell antigens defined by monoclonal antibodies: the 65,000-dalton antigen of T cells (T65) is also found on chronic lymphocytic leukemia cells bearing surface immunoglobulin.
Peripheral blood lymphocytes from 15 patients with chronic lymphocytic leukemia (CLL), four patients with lymphosarcoma cell leukemia (LCL), four patients with hairy cell leukemia, and three patients with a monoclonal gammopathy (two with IgM, one with IgA) were tested for reactivity with the anti-T cell monoclonal antibody, T101. By immunofluorescent staining, all of the patients had circulating monoclonal surface Ig+ (sIg+) lymphocytes except for three CLL patients whose leukemia cells were sIg-. The leukemia cells of all of the sIg+ CLL cases were reactive with T101 antibody by indirect immunofluorescence; however, the abnormal cells in all of the remaining cases were unreactive. Reactivity of sIg+ CLL cells with T101 was confirmed by a radioactive binding assay, absorption analysis, and complement-dependent cytotoxicity. Moreover, a 65,000-dalton protein (T65), similar to that found on T cells, was precipitated by T101 antibody from the surface of sIg+ CLL cells. The fluorescent staining of sIg+ CLL cells by T101 antibody was weak as was the staining of the sIg. This was in contrast to the LCL cells, which had intense staining sIg and absence of staining with T101 antibody. These data demonstrate the existence of two major subtypes of CLL that have phenotypes sIg+ and T101+ and sIg-T101-. The implication of the finding of dual T and B markers on the major type of CLL, but not other B cell malignancies is discussed.
Absorption↗
Tumor-associated antigens of chemically-induced murine tumors; the emergence of MuLV and fetal antigens after serial passage in culture.
Using radioiodinated Staphylococcus aureus protein A [125I]SPA to measure syngeneic, allogeneic and heterogeneic IgG bound to murine tumor cells, we performed a serological analysis of surface antigens of 8 solid tumors and 2 leukemias of BALB/c mice (3 chemically-induced colon carcinomas, 3 chemically-induced sarcomas, 1 murine leukemia virus (MuLV) induced leukemia, 1 irradiation induced leukemia, 1 spontaneous melanoma and 1 spontaneous sarcoma). We were able to detect and distinguish between at least five separate antigenic specificities on these tumors. Unique tumor-associated antigens were found on 3 of the tumors, MuLV related antigens on 8 tumors, fetal antigens on 7 tumors and two distinct common antigens on 7 tumors (common antigen 1 (CA-1) on 5 tumors and common antigen 2 (CA-2) on 2 tumors). Neither of the common antigens was found to be sarcoma, carcinoma or tissue-tupe specific. A number of tumors which did not originally express either MuLV or fetal antigens in primary cultures expressed these antigens after several serial passages in vitro.
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Antigenic properties and molecular weights of murine leukemia virus-binding proteins.
A murine T lymphoma cell line, WEHI-22, has been studied for the presence of murine leukemia virus-binding proteins and for the presence of cell surface molecules that share antigens with mouse immunoglobulins. With surface radioiodination, detergent disruption, and immunoprecipitation, a 60 to 70,000-dalton molecule has been described that is recognized by chicken anti-mouse immunoglobulin serum. In competition experiments this molecule cross-reacts with highly purified mouse IgM myeloma proteins. A cell surface molecule of similar size can be shown to bind to mouse leukemia viruses. Pre-precipitation of the WEHI-22 cell surface material with chicken anti-mouse immunoglobulin removes the material binding to leukemia viruses.
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