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G Klein

Publications and source records attributed to G Klein.

At least 973 records · Page 54Linked to original sources
PubMed1979

Detection of virus and cellular-determined antigens in situ using [125I]protein A and autoradiography.

The present paper describes the use of [125I]Protein A, isolated from Staphylococcus aureus, in detecting antigen-antibody complexes by autoradiography on single cells. the method is relatively quick, reproducible, potentially more sensitive than immunofluorescence, and should be useful in combination with conventional radioimmuno-assays. We have used it to detect the cellular expression of IgM, kappa, lambda, and beta 2-microglobulin, as well as the expression of Epstein-Barr Virus (EBV)-associated antigens expressed in human lymphoblastoid cell lines.

Antigens, Viral↗
PubMed1979

Nonrandom chromosome changes involving the Ig gene-carrying chromosomes 12 and 6 in pristane-induced mouse plasmacytomas.

The karyotypes of pristane-induced mouse plasmacytomas were studied by G banding. Only primary tumors or early passage generations were analyzed. In contrast to murine T cell leukemias that showed a regular trisomy of chromosome 15, all plasmacytomas showed a consistent translocation of the distal part of chromosome 15 to either chromosome 6 [rcpT(6;15)] or 12 [T(12;15)]. The specific breakpoints were at 6C, 15D3/E ro D2/3 and 12F2. Early passage generations often showed a mixed population with two different translocations, suggesting polyclonal origin. Considered together with the known karyotypic features of murine and human lymphomas, these findings support the theory that the nonrandom chromosomal changes in lymphoproliferative malignancies are associated with the type of the target cell, rather than with the etiological agent. Moreover, the involvement of the chromosomes known to carry the heavy chain (12) and the light chain (6) determinants, respectively, raises the question of whether the translocations may be related to the DNA level rearrangements known to occur during the differentiation of normal plasma cells.

Animals↗
PubMed1979

The EBV-carrying, beta2M/HLA deficient Burkitt lymphoma line Daudi is sensitive to EBV-specific killer T-cells of mononucleosis patients.

The beta2-microglobulin/HLA deficient Burkitt lymphoma line Daudi was tested for sensitivity to EBV-specific cytotoxicity mediated by natural killer (NK)-depleted T-cells from acute mononucleosis patients. While the Daudi line was not as sensitive as the reference EBV-genome-positive target line, it was clearly sensitive in the majority of cases. This would speak against a major role of syngeneic restriction in this system.

Burkitt Lymphoma↗
PubMed1979

Evidence for antigenic distinctness of the Epstein--Barr virus-determined nuclear antigen and the Herpesvirus papio-determined nuclear antigen.

Previous serological evidence indicated that Epstein--Barr virus-determined nuclear antigen (EBNA) has cross reactive components with the herpesvirus papio-determined nuclear antigen (HUPNA) and, in addition, it has distinct components of its own, not present in HUPNA. In the present study, this hypothesis was studied by absorption experiments. Absorption of anti-EBNA positive human sera with EBNA abolished both anti-EBNA and anti-HUPNA reactivity. Absorption with HUPNA removed all anti-HUPNA reactivity but did not reduce anti-EBNA to any detectable degree, thus confirming the hypothesis.

Animals↗
PubMed1979

Is trisomy cause or consequence of murine T cell leukemia development? Studies on Robertsonian translocation mice.

Trypsin-Giemsa banding studies on T cell leukemias induced in Robertsonian translocation mice by dimethylbenz[a]anthracene and Moloney leukemia virus show a trisomy of chromosome 15 even in cases in which chromosome 15 has undergone centromeric fusion with chromosomes 1, 5, or 6. These results suggest that the duplication of gene(s) located on chromosome 15 is of critical importance for murine T cell leukemia development.

Animals↗
PubMed1979

Detection of a nuclear antigen in Herpesvirus ateles-carrying marmoset lines by the acid-fixed nuclear binding technique.

In vitro binding of a Herpesvirus ateles (HVA)-associated soluble antigen to amphibian erythrocyte nuclei was demonstrated by the acid-fixed nuclear binding technique in combination with anticomplement immunofluorescence. Incubation of concentrated salt-extracted soluble antigens derived from HVA-carrying marmoset lines with methanol/acetic acid-fixed erythrocytes of frogs and salamanders resulted in a brilliant nuclear fluorescence after exposure to a live virus-boostered, anti-HVS-positive squirrel monkey serum. Anti-HVS-negative sera did not stain. The activity of the positive serum could be abosrbed completely with extracts of HVA-carrying cells but not with Epstein-Barr virus-carrying or Herpesvirus papio-carrying cells. The HVA-associated antigen was also present in lytically HVA-infected marmoset kidney cells.

Animals↗
PubMed1979

Lymphoma development in mice and humans: diversity of initiation is followed by convergent cytogenetic evolution.

Human B cell lymphoma and murine T cell leukemia can be initiated by several agents. The present paper formulates some thoughts on the role of cytogenetic changes in the subsequent neoplastic process. Initiation creates long-lived preneoplastic cells. In some respects, they are comparable to in vitro-transformed ("immortalized") cell lines that maintain a diploid karyotype and are not tumorigenic in vivo. The development of a tumorigenic ("autonomous") clone is dependent on additional changes at the genetic level. In human B and murine T cell lymphoma, there are characteristic nonrandom chromosomal changes. The 14q+ marker appears to play a key role in human B cell lymphomas. The reciprocal 8;14 translocation in Burkitt lymphoma is a specialized subclass within this category. In murine T cell leukemia, trisomy 15 is the predominant change. The clustering of these nonrandom changes to tumors derived from a certain cell type rather than to tumors induced by a given etiological agent has important implications for the understanding of the genetic control of cellular responsiveness to growth-regulating forces in vivo.

AKR murine leukemia virus↗
PubMed1979

Serologically defined, unique surface antigen on a mouse mammary adenocarcinoma.

Syngeneic A.SW mice were immunized with sublethal viable cells of a spontaneous mammary adenocarcinoma S3W. The serum was tested by complement-dependent cytotoxicity against in vitro-cultured S3W cells and a spectrum of controls. S3W cells were found to react with at least four different kinds of antibodies in the serum. One antigen was present on several leukemia cell lines. A second cross-reactive antigen was detected on polyoma virus-induced tumors. A third was demonstrated on other mammary carcinoma lines and in a sarcoma of C3H origin. Following the removal of all three antibodies by absorption with the appropriate cross-reactive target cells, a fourth antibody remained that gave a strong cytotoxic reaction with S3W but with no other target line tested.

Adenocarcinoma↗
PubMed1979

Establishment of anti-TNP antibody-producing human lymphoid lines by preselection for hapten binding followed by EBV transformation.

Human lymphoblastoid cell lines that produce specific antibody against the hapten trinitrophenyl (TNP) have been established by selecting TNP-binding human B lymphocytes by TNP-rosetting and Ficoll-Isopaque separation, followed by Epstein-Barr virus (EBV) immortalization. Derived lines secreted polyclonal anti-TNP antibodies and contained relatively small numbers of specific rosette- and plaque-forming cells against TNP-RBC. Following rerosetting with TNP-RBC, the frequency of rosette-forming cells increased from 2% to 75%. In parallel, the frequency of plaque-forming cells increased from 0.4% to 30%. The antibody titres in the supernatants increased from 64 to 512 and from 48 to 192, as measured by TNP agglutination and haemolytic assays, respectively. The antibodies were 19S, IgM. The specificity of the anti-TNP antibody was confirmed by the hapten inhibition test, in comparison and cross-reactivity tests with the supernatant of the previously established, EBV-transformed anti-4-hydroxy-3,5-dinitrophenacetic acid (NNP) antibody-producing cell line. Both antibodies were specific: the homologous hapten inhibited them but the heterologous hapten did not.

Antibodies↗
PubMed1979

Immunochemical characterization of Epstein-Barr virus-associated early and late antigens in n-butyrate-treated P3HR-1 cells.

Sodium butyrate induces the Epstein-Barr virus cycle in latently infected P3HR-1 cells with a high efficiency. This fact was utilized for the metabolic labeling of the Epstein-Barr virus antigens. Nonproducer Raji cells, lacking both early antigen and viral capsid antigen, were used as controls. Immunoprecipitation patterns were compared with 13 anti-Epstein-Barr virus (viral capsid antigen) - positive and 3 negative sera. Sixteen polypeptides were identified as being associated with the lytic Epstein-Barr virus cycle. Their molecular weights ranged from 31,000 (31K) to 275K on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Two polypeptides, 158K and 165K, could be classified as late viral products on the basis of their sensitivity to cytosine arabinoside. Six of the polypeptides, i.e., 90K, 95K, 134K, 165K, 236K, and 275K, were detected by [(3)H]glucosamine labeling. Among the early, cytosine arabinoside-insensitive polypeptides detected by [(35)S]methionine labeling, a 152K component appears to be a major constituent of early antigen. This polypeptide was precipitated by all anti-Epstein-Barr virus-positive sera tested. As a rule, together with the 103K and 134K polypeptides, the 152K component is precipitated by anti-early antigen, R (restricted) antibodies. In addition, anti-early antigen D (diffuse) antibodies precipitate 31K, 51K, 65K, and 90K components.

Antigens, Viral↗