Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A BALB/c B cell lymphoma, 2PK-3, was found to be activation lymphocyte alloantigen (Ala-1)-positive by virtue of its ability to absorb out the cytotoxic anti-Ala-1.1-like antibody activity of an antiserum against activated BALB/c (Ala-1.1) lymphocytes. Injection of 2PK-3 cells from the spleens or ascites of lymphomatous BALB/c mice into H-2d compatible DBA/2 mice led to the rapid development of an antiserum with properties identical to anti-Ala-1.1 alloantisera. Thus, it did not significantly kill normal spleen cells from any one of 7 different strains tested, but killed over 85% of Con A- or LPS-stimulated spleen cells of 4 Ala-1.1 positive strains; activated lymphocytes of Ala-1.2 were not affected. Furthermore, these properties were seen with unabsorbed antisera. The results indicate that the Ala-1 phenotype may, in some cases, be retained on neoplastic lymphocytes and that such cells, being rapidly and easily obtained in vivo in large quantities, can serve as a convenient source of immunogen for the development of anti-Ala-1 alloantisera in certain donor-recipient combinations.
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PMID:A simple and convenient method for producing anti-activated lymphocyte alloantisera which does not require prior absorption. 65 95

Supernatants from four murine B and one T-cell lymphoma cultures were tested for their suppressive effect on allogeneic response in vitro (MLR), on their effect on mitogenic response to ConA and LPS and on their effect in vivo on allogeneic stimulation of BALB/c mice by C57BL/6J spleen cells. Two out of four B-cell supernatants (WEHI-231 and 24-666) were also tested for their effect on induction of IL-2 like activity by ConA in BALB/c spleen cells and on the effect of their injection on subsequent allogeneic response of spleen cells from BALB/c mice immunized against C57BL/6J spleen cells. The supernatants from all lymphoma lines inhibited MLR but only supernatants from the B-cell lymphoma lines also inhibited mitogenic stimulation in vitro and allogeneic immunization. The two B-cell supernatants tested also inhibited induction of IL-2 like activity and decreased the ability of spleen cells from the injected mice to respond to allogeneic stimulation. Partial characterization of supernatants from WEHI-231 and 24-666 lymphoma cultures revealed the non-protein nature of the suppressor factor(s), indicated a molecular weight of less than 5 Kd and suggested a ganglioside or a sialyated glycoproteinic nature.
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PMID:Immunosuppression in vitro and in vivo by supernatants from murine lymphoma cell lines. 153 68

Injection of a nonlymphomagenic ecotropic virus 24-666 isolated from a B cell lymphoma of AKR origin into young AKR mice (1-60 days old) inhibited spontaneous T cell lymphoma development. The reduction in T cell lymphoma incidence (16/106-15%) was accompanied with the appearance of B cell lymphomas (16/106-34%) in older mice (500 days mean latency). Infection of newborn to 60-day-old AKR mice with 24-666 prevented changes in thymus subpopulations and expression of MuLV-related cell surface antigens, normally observed in the thymus of 5- to 6-month-old AKR mice prior to lymphoma development. Thymuses of 24-666-infected 9- to 12-month-old mice lacked recombinant dual tropic virus (DTV) expression and retained the thymus pattern of 2-month-old AKR mice. At 12 months after 24-666 administration a striking decrease in Thy1.1 level and in the CD4+ CD8+ population and an increase in CD4- CD8- cells and in mu+ B cells, predominantly Ly1+, were observed. The presence of B cells in these thymuses was also reflected in the high response of thymocytes to LPS blastogenesis accompanied by a decreased response to PHA. Although T cell lymphoma development was markedly reduced by 24-666 administration, the establishment of potential lymphoma cells (PLC) was not affected. Transfer of lymphoid cells from 12-month-old grossly normal 24-666-infected mice to the appropriate recipients resulted in a high incidence (64-80%) of B cell lymphoma development. Thus, 24-666 seems to act through interference with the establishment of DTV in the thymus, thereby preventing PLC promotion to overt T cell lymphomas. Lack of the favorable microenvironment for PLC development in the T cell pathway enables PLC development in the B cell pathway in older mice.
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PMID:Prevention of spontaneous AKR T cell lymphomagenesis by 24-666, a virus isolated from an AKR B cell lymphoma. 167 38

Little is known about the role of signals transduced by cell surface IgM (sIgM) expressed during early B cell development. A subclone (1.6) of the late pre-B cell lymphoma 70Z/3.12 was used to study signal transduction by surface mu heavy (H) chain before and after transition to the early immature B cell stage, and the functional consequences thereof. Although kappa L chain expression can be induced on 1.6 cells by LPS or cytokines, immunoprecipitations indicated that the non-induced 1.6 cells expressed mu H chain with an alternative protein(s) which may be a surrogate light chain(s). Consistent with this, anti-mu but not anti-kappa or anti-lambda antibodies caused transient Ca2+ mobilization in noninduced 1.6 cells. The Ca2+ signal was derived from both intracellular stores and Ca2+ influx in either noninduced cells or in cells that had been preinduced to express kappa L chain. Thus, the ability of mu H chain to mobilize Ca2+ as a second messenger does not depend upon the expression of mature L chains. The immature B lymphomas, WEHI-231 and CH1, express mature forms of IgM and undergo growth arrest when stimulated by anti-mu antibody. In contrast, signals generated by mu H chain on either noninduced or preinduced 1.6 cells or in the sIgM+ pre-B cell transfectant 300-19 mu lambda 36/8 did not cause growth arrest. These results suggest that mu H chain expressed on pre-B cells is capable of mobilizing Ca2+, but that this signal alone is insufficient to induce growth arrest in the pre-B cell.
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PMID:Surface mu heavy chain expressed on pre-B lymphomas transduces Ca2+ signals but fails to cause growth arrest of pre-B lymphomas. 172 70

A 72/74-kDa peptide binding protein (PBP72/74) was previously described which plays a role in the processing and/or presentation of Ag, possibly by facilitating the association of processed Ag with the MHC class II molecules. PBP72/74 was recently shown to be related to the 70-kDa family of heat shock proteins (hsp70), whose members show the general characteristic of binding to denatured or inappropriately folded proteins. Here we describe the cellular and subcellular distribution of PBP72/74. By flow cytometry with PBP72/74-specific rabbit antisera, PBP72/74 is detected on the surfaces of mouse Ig+ B cells and MAC-1+ macrophages. PBP72/74 74 was not detected on the surfaces of Thy-1+ T cells or NK1.1+ NK cells. The cell surface expression of PBP72/74 does not require MHC class II expression. Indeed, the Ia- variant B cell lymphoma cell line, M12.C3, expresses PBP72/74 at levels equivalent to that of the Ia+ parent cell line, M12.4.1, from which it was derived. Furthermore, the fibroblast L cell line, DAP.3, shows no cell surface expression of PBP72/74, nor do DAP.3 lines transfected with and expressing genes encoding the alpha- and beta-chain of the I-Ad and I-Ed molecules. Moreover, treatment of B cells with either IL-4 or LPS, which increases Ia expression severalfold, does not affect PBP72/74 expression. Thus, PBP72/74 cell surface expression appears to be a property of B cells and macrophages, independent of Ia expression. In addition, the B cell surface expression of PBP72/74 is not altered by stress in the form of heat shock. Thus, PBP72/74 appears to be a constitutive noninducible member of the hsp70 family. By immunoelectron microscopy, PBP72/74 is detected in approximately 36% of early endocytic vesicles into which surface Ig is internalized after binding to anti-Ig antibodies. This compartment was previously shown to contain class II en route to the cell surface associated with invariant chain and the proteases cathepsin B and D and is suggested to be a subcellular site of antigen processing. PBP72/74 is also found associated with the plasma membrane, endoplasmic reticulum, and membranes proximal to the Golgi stacks. The cellular and subcellular distribution of PBP72/74 is consistent with its playing a role in the processing of presentation of Ag with the MHC class II molecules.
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PMID:Cellular and subcellular distribution of PBP72/74, a peptide-binding protein that plays a role in antigen processing. 198 75

We have previously shown that the steady state levels of transcripts encoded by an endogenous mouse mammary tumor virus (MMTV) increase during LPS-induced differentiation of both normal B lymphocytes and an inducible B cell lymphoma, CH12. A large body of evidence suggests that MMTV expression is primarily limited to mammary tissues and that expression in cell lines from nonmammary tissues is accompanied by viral amplification and alterations in the transcriptional control regions of the viral long terminal repeat. We have, therefore, carefully characterized MMTV expression in CH12 cells and in other cells of the B lineage in order to determine if the expression of MMTV transcripts in differentiating B cells results from the "abnormal" transcriptional regulation seen in other nonmammary tissue. In this manuscript, we present evidence that MMTV transcripts are expressed in a variety of cells of the B lineage and that the levels of constitutive expression vary among the different cells. On the other hand, T cell lymphomas lacking amplified MMTV do not contain proviral transcripts, suggesting that MMTV transcription may be preferentially expressed in B lymphocytes. We demonstrate that MMTV transcripts are up-regulated during cytokine-mediated as well as LPS-mediated differentiation, and that most, if not all, expression is due to the activity of a single proviral gene, Mtv-9, in CH12 cells. Furthermore, the expression of MMTV transcripts in CH12 cells neither requires nor is accompanied by amplification of the provirus. Sequence analysis demonstrates that the U3 region of the expressed Mtv-9 long terminal repeat contains neither deletions nor insertions, and the well-characterized enhancer and promoter sites in the glucocorticoid response element which are known to be involved in transcriptional regulation of MMTV in mammary tissues have not been disrupted. These data suggest that the Mtv-9 locus behaves as a normal somatic gene which is differentially regulated during B cell development and differentiation. Unlike the events which lead to MMTV expression in other nonmammary tissues, B cells may express transcription factor(s) which are capable of inducing expression of endogenous MMTV proviral genes during the natural course of differentiation. Analysis of the mechanisms which control the expression of this gene should be useful in characterizing the molecular events which govern B cell differentiation.
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PMID:Molecular events in B lymphocyte differentiation. Inducible expression of the endogenous mouse mammary tumor proviral gene, Mtv-9. 215 65

NBL is a spontaneous B cell lymphoma that originated in NIH Swiss nude mouse, and has been maintained as an in vitro line for 4 yr in our laboratory. It is surface IgM positive and expresses several B cell markers including Fc receptors, as well as Ly-1. Although clones of NBL will grow in serum-containing medium, this cell line enters a quiescent state in serum-free culture. However, in the presence of affinity-purified or monoclonal anti-mu reagents, NBL increases its rate of proliferation as measured by thymidine incorporation or in absolute cell numbers. This stimulation is specific for mu-chain, because it does not occur with anti-beta 2 microglobulin, irrelevant nonbinding antibodies, or with monoclonal anti-B cell lineage markers. Bivalent anti-mu is required, and no consistent Fc-mediated inhibition of growth has been detected. Stimulation of NBL occurs optimally at critical cell densities (greater than 3 X 10(3)/well) in the absence of serum. Therefore, we reasoned that NBL either produced or was receptive to known B cell growth factors. Although no classic IL 1 was detected in NBL supernatants, some BCGF-I-like activity was found. Finally, in the presence of LPS, both spontaneous and anti-mu-stimulated NBL growth was inhibited, a result suggesting maturation of this lymphoma. These results suggest that NBL represents an excellent model to study the growth and differentiation of B cell subsets.
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PMID:Lymphoma models for B cell activation and tolerance. I. Conditions for the anti-mu-dependent stimulation of growth in NBL, a nude B cell lymphoma. 257 9

We have identified a gene whose expression appears to be associated with a late stage in the differentiation of B lymphocytes into antibody secreting cells, as shown by using the inducible B cell lymphoma, CH12. Restriction mapping and partial sequencing of a cDNA clone isolated by subtraction analysis demonstrated that the clone, SC34, represents an envelope (env) gene transcript of a mouse mammary tumor virus (MMTV). In CH12 cells and in normal B cells, levels of MMTV RNA were increased after stimulation with LPS. The env transcript was the predominant MMTV RNA species and increased more dramatically than did levels of the genomic transcript. In differentiating CH12 cells, env transcripts increased as much as 20-fold above levels found in replicating, antibody nonsecreting CH12 cells. The major increase in expression appeared to be associated with B cell differentiation and not replication. By Southern blot analysis, only bands characteristic of endogenous proviruses were found in CH12, indicating that viral sequences were not amplified in this cell line. Restriction mapping indicated that the SC34 cDNA clone was a product of the Mtv-9 locus. Mtv-9 previously was shown to encode a complete MMTV provirus on chromosome 12, on which Ig heavy chain genes also are located. Increases in MMTV transcripts followed distinct kinetics and were quantitatively different from changes in immunoglobulin gene products. The expression of env RNA appears to more accurately reflect differentiation to antibody secretion in CH12 cells than does the expression of immunoglobulin gene transcripts.
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PMID:Molecular events during B lymphocyte differentiation. Induction of endogenous mouse mammary tumor proviral envelope transcripts after B cell stimulation. 284 1

In order to study T cell regulation of B cell isotype differentiation we have developed a model system consisting of clonal populations of T and B cells. Using this system we have shown that the murine B cell lymphoma, 70Z/3, can be induced to express membrane IgG2b by exposure to a T cell hybridoma derived from the Peyer's patch (termed HAJ-3). The membrane bound IgG2b (mIgG2b) expression is associated with induction of gamma 2b-mRNA, but switch region rearrangement and C mu deletion does not occur. While LPS-stimulated 70Z/3 B cells also express considerable amounts of gamma 2b-mRNA they do not express detectable mIgG2b, indicating that T cell influence is necessary for the production of translatable gamma 2b-specific mRNA. Both the LPS and T cell induced gamma 2b mRNA transcripts lack VH sequences, implying that the surface IgG2b detected lacks a variable region. These findings lend support to a two step model of B cell isotype switching and provide evidence that T cells can regulate early events involved in B cell isotype differentiation.
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PMID:Molecular analysis of membrane gamma 2b heavy chain expression. 289 38

Supernatants containing lymphotoxin (LT) and immune interferon (IFN-gamma) or IFN-gamma alone were produced by antigen-stimulated murine T cell clones. These lymphokine preparations as well as cloned recombinant murine IFN-gamma (Genentech) were tested for antiproliferative activity on a variety of murine T, B, macrophage, and mastocytoma tumors and on T cell clones and LPS-stimulated B cells. The growth of every cell line tested was susceptible to the LT-containing supernatants. Cloned recombinant murine IFN-gamma inhibited the growth of A9 fibroblasts but not L929 cells. Neither the cloned murine IFN-gamma nor that produced by a T cell clone had any appreciable effect on the lymphoid cells except for one B cell lymphoma, A20. The sensitivity of nontransformed T and B cells to LT indicates that this lymphokine may play an immunoregulatory role. Indeed, the T cells that produce LT are sensitive to its cytotoxic activity and, therefore, regulate themselves. The differential inhibitory effects of LT and IFN-gamma on lymphoid target cells allow us to distinguish between preparations that contain IFN-gamma alone and those that contain LT and IFN-gamma. The susceptibility of lymphoid tumors to the antiproliferative activity of the LT-containing preparations indicates that LT either alone or together with IFN-gamma may be useful in tumor therapy.
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PMID:The differential inhibitory effect of lymphotoxin and immune interferon on normal and malignant lymphoid cells. 298 82


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