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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 switch variant of the I.29 murine B-cell lymphoma expressing membrane IgE and inducible by lipopolysaccharide (LPS) to increase the rate of IgE secretion was characterized. The cells (I.29 epsilon +2) express membrane-bound IgE, and also secrete considerable amounts of IgE when grown in regular culture medium. Membrane and secreted IgE contain structurally different heavy chains. The former is constituted by a 93-kd molecule (epsilon m), while secretory chains (epsilon s) have an apparent mol. wt of 86,000. Both epsilon m and epsilon s are heavily glycosylated: in the presence of tunicamycin their apparent mol. wt is reduced by approx. 35% (61 kd for epsilon m and 56 kd for epsilon s). Glycosylation is necessary for membrane expression and for secretion of IgE molecules. Stimulation with LPS leads to the disappearance of IgE molecules from the cell surface (determined by radioiodination) although epsilon m-chains are still synthesized, suggesting a defective transport of membrane IgE in LPS-treated cells. The epsilon m:epsilon s ratio decreases upon LPS stimulation. A similar change can be observed in the messenger RNAs specific for epsilon m and epsilon s, possibly suggesting a major pretranslational control for epsilon m and epsilon s biosynthesis.
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PMID:Biosynthesis of membrane and secreted epsilon-chains during lipopolysaccharide-induced differentiation of an IgE+ murine B-lymphoma. 393 17

The transcriptional activity of the kappa immunoglobulin genes in a B-cell lymphoma line, 7OZ/3 was measured before and after stimulation by lipopolysaccharide (LPS). Analyses of accumulated nuclear RNA components and of nascent transcripts showed that LPS induces transcription of both the productively rearranged (kappa+) and the unrearranged (kappa) allele in these cells. This pattern of transcriptional activation correlates well with the LPS induced appearance of a DNAase I hypersensitive site on both alleles in the vicinity of a putative enhancer element (Parslow and Granner, Nucl. Acids Res. 11, 4775, 1983). However, the transcriptional activation is not accompanied by detectable hypomethylation at Hha I and Hpa II sites which are normally undermethylated when kappa genes are constitutively expressed. These findings have enabled us to evaluate the relative importance of various structural parameters to the transcriptional competence of the kappa locus.
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PMID:Lipopolysaccharide-induced transcription of the kappa immunoglobulin locus occurs on both alleles and is independent of methylation status. 632 27

The cultured murine B cell lymphoma, 70Z /3, can be induced to express membrane IgM ( mIgM ) after exposure to lipopolysaccharide (LPS) or T cell-derived factors. The kinetics and magnitude of the responses have been compared in wild type 70Z /3 cells and three variants by using flow cytometric analysis and immunoprecipitation. Wild type 70Z /3 cells respond to LPS more quickly and with twofold greater mIgM than to concanavalin A-induced spleen cell supernatant (CAS). Variants were selected for their abnormal mIgM expression in response to LPS, but individual variants also showed normal, aberrant, or no response to CAS. When cells were induced with suboptimal amounts of LPS and CAS, a synergistic effect on the magnitude of mIgM expression was seen in wild type and variant cells. This suggests that both inducing agents are utilizing some part of a common inductive mechanism. The different responses of the variant cell lines will allow further genetic dissection and comparison of the mIgM expression pathways used in response to LPS and CAS.
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PMID:Comparison of membrane IgM expression in the murine B cell lymphoma 70Z/3 treated with LPS or supernatant containing T cell factors. 642 42

The B cell lymphoma WEHI 231 has been previously characterized as resembling a resting B cell, bearing large amounts of IgM on the cell surface, but not secreting immunoglobulin. When WEHI 231 cells were cultured together with low concentrations of lipopolysaccharide (LPS) (0.01 to 3 micrograms/ml), increased levels of immunoglobulin were detected in culture supernatants. Analysis by immunoprecipitation and gel electrophoresis demonstrated that this was secreted (19S) IgM. It was noted that small amounts of secretory IgM were produced even in control cultures not deliberately exposed to LPS. Analysis of the cell lysates showed that LPS treatment resulted in a reduction of synthesis of the surface form of IgM. In contrast, the cytoplasmic pool of IgM precursors was considerably expanded by LPS treatment, reflecting the overall increase in synthesis of IgM in LPS-treated cells. These changes in IgM metabolism appear to parallel closely those occurring in normal B cells after mitogen or antigen challenge. This cloned tumor line promises to be a valuable system in which to investigate some of the molecular events in B cell differentiation.
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PMID:The regulation of growth and differentiation of a murine B cell lymphoma. I. Lipopolysaccharide-induced differentiation. 678 55

WEHI 231 is a murine B cell lymphoma, which from our previous studies is highly susceptible to a lipopolysaccharide (LPS) induced differentiation signal. In this paper we show that anti-immunoglobulin (Ig) antibody at low concentrations (0.1 micrograms/ml) inhibits cell proliferation and results in cell death. Heterologous sera specific for mu- and kappa-chains, and a monoclonal antibody (E4) developed in our laboratory and specific for mu-chain, profoundly suppressed the growth of WEHI 231 in both soft agar culture and liquid culture. The F(ab')2 fragments were as potent as intact Ig, indicating that neither Fc receptor binding nor complement activation were required for this inhibition of growth. Neither heterologous antibodies that bound to WEHI 231 but not to the Ig receptor, nor a monoclonal antibody that bound to non-Ig cell surface structures (a brain-associated antigen) inhibited the growth of WEHI 231. LPS did not prevent inhibition of growth by anti-Ig antibody, and even when addition of LPS preceded the addition of anti-Ig, profound inhibition occurred. WEHI 231 thus promises to be a convenient tool for investigating the mechanism of signal transmission by the Ig receptor.
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PMID:The regulation of growth and differentiation of a murine B cell lymphoma. II. The inhibition of WEHI 231 by anti-immunoglobulin antibodies. 678 56

Recently, we have described that anti-IgM antibodies profoundly inhibited the growth of BKS-2, an immature B cell lymphoma. In this report, we demonstrated that ionomycin alone at very low concentrations (20 nM) inhibited the growth of BKS-2 cells completely. The levels of intracellular Ca2+ induced by the inhibitory concentrations of ionomycin were comparable to those in anti-IgM-treated cells. The growth inhibition caused by ionomycin was reversed by phorbol 12-myristate 13-acetate and lipopolysaccharide. In addition, the immunosuppressants, cyclosporin A and FK506 conferred significant protection from the negative signal induced by ionomycin. However, either cyclosporin A, FK506 or lipopolysaccharide was not found to have direct effect on ionomycin-induced Ca2+ mobilization in BKS-2 cells. Also, ionomycin augmented the anti-IgM-induced growth arrest in these cells. Furthermore, BKS-2 cells that were exposed to anti-IgM or ionomycin underwent apoptosis as characterized by DNA fragmentation. Thus, the characteristics of growth inhibition induced by ionomycin and anti-IgM appeared to be similar in that phorbol 12-myristate 13-acetate, lipopolysaccharide, cyclosporin A and FK506 caused significant reversal from such negative signals and both ionomycin and anti-IgM induced apoptosis in these cells. Altogether, these results showed that the elevation of intracellular Ca2+ alone was sufficient to inhibit the growth of some B lymphoma cells.
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PMID:Elevation of cytosolic calcium is sufficient to induce growth inhibition in a B cell lymphoma. 769 6

The kappa immunoglobulin (Igk) light chain locus is transcriptionally silent in the mouse B-cell lymphoma 70Z/3. However, exposure to lipopolysaccharide (LPS) or interferon-gamma (IFN) causes a marked increase in Igk transcription. By immunoselection, we isolated two variants that are nonresponsive to IFN. One variant, AT7.2, has retained its response to LPS (IFN-LPS+), whereas the other, AT3.3, is also nonresponsive to LPS (IFN-LPS-). Stable transfection of an intact Igk gene does not rescue the phenotype of either variant. Both variants have intact Igk genes and neither is deficient in the binding or uptake of IFN. Nuclear extracts from LPS-treated wild-type 70Z/3 cells show strong increases in three transcription factors: OTF-2, NF-kappa B, and kBF-A. Remarkably, when the IFN-LPS- variant is treated with LPS, all three transcription factors are still observed in the nuclear extracts. Treatment of wild-type cells with either LPS or IFN also causes a decrease in nuclear complexes that bind to two other regions of the Igk intron enhancer, the octenh and the E kappa MHCIC regions. Both of these changes are also observed after LPS or IFN treatment of the IFN-LPS- variant. Thus, this variant transduces the IFN and LPS signals at least into the nuclear compartment, but still fails to activate Igk transcription. In contrast, the IFN-LPS+ variant decreases neither the octenh nor the E kappa MHCIC binding complexes in response to IFN. This variant may be defective in transducing the IFN signal to the nucleus. These variants will be useful in studying the activation of Igk transcription and the IFN signaling pathway in B cells.
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PMID:Two different IFN-gamma nonresponsive variants derived from the B-cell lymphoma 70Z/3. 803 28

IL-12 has been shown to play a central role in cell-mediated inflammatory reactions through direct activation of T cells and NK cells. IL-12 also strongly influences humoral immunity but these effects have been thought to be indirect and caused by intermediary cytokines. Using flow cytometry, we now show that IL-12 directly interacts with B cells. Freshly isolated murine peritoneal B-1 and conventional B lymphocytes bound IL-12, but splenic B cells failed to react unless first stimulated with lipopolysaccharide. All murine B cell sources were found to express IL-12R beta 1 subunit transcripts as detected by PCR and RNase protection assays. IL-12 binding was also detected on phytohemagglutinin-stimulated human T cell blasts and Staphylococcus aureusl IL-2-stimulated B cell blasts but not on freshly isolated peripheral blood lymphocytes. Similarly, IL-12 directly bound to the human SKW6.4 Burkitt's B cell lymphoma line. In all cases positive staining was ablated by omitting IL-12 from the procedure, showing that it was not due to detection of endogenous IL-12. These findings indicate that B cells represent another major target for IL-12 in addition to T and NK cells, and that IL-12 can directly affect humoral immunity.
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PMID:Direct binding of IL-12 to human and murine B lymphocytes. 898 80

The results of cytogenetic studies are reported in 76 patients with B-chronic lymphoproliferative disorders (B-CLPD): 60 patients with chronic lymphocytic leukemia (CLL), six with follicular lymphoma in leukemic phase (FLLP), five with splenic B-cell lymphoma with villous lymphocytes (SLVL), two with chronic prolymphocytic leukemia (CPL), two with hairy cell leukemia (HCL), and one with plasma cell leukemia (PCL). PHA (phytohemagglutinin), PWM (pokeweed mitogen), LPS (lipopolysaccharide from Escherichia Coli), TPA (phorbol 12-myristate acetate), IL6 (interleukin 6), and DxS (dextran sulfate) were used as mitogens. Mitoses were obtained in 75 cases. Clonal aberrations could be demonstrated in 34 cases (44%). In CLL, classical type, chromosomes 6, 11, and 13 were more frequently involved, whereas trisomy 12 was frequently found in CLL mixed-cell type, in FLLP, and CPL. In SLVL the deletion del(7)(q32) is noteworthy and miscellaneous chromosome abnormalities in the remaining patients were observed. Regarding the efficiency of mitogens, PHA turned to be the most effective in obtaining metaphases and in detecting clonal chromosomal aberrations.
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PMID:Cytogenetic studies in seventy-six cases of B-chronic lymphoproliferative disorders. 907 2

Murine lymphocytes are relatively refractory to efficient transfection or retroviral gene transduction. Adenovirus has been used as a vector to transduce a wide variety of cell types. Several advantages of adenoviruses are their ability to transduce non-cycling cells and to transduce the majority of cells in a population. Unfortunately, lymphocytes are not susceptible to infection with conventional adenovirus. Therefore, to express genes efficiently in murine B cells, we tested the ability of genetically modified adenovirus to transduce the beta-galactosidase gene. We found that adenovirus containing polylysine in the fiber knob was able to efficiently transduce lipopolysaccharide (LPS)-activated splenic B cells and the B lymphoma line M12.4.1; greater than 80% of the cells expressed beta-galactosidase activity. However, small resting B cells did not express activity unless treated with LPS after infection. This transduction was mediated by interaction with charged molecules since heparan-sulfate, and to a lesser degree chondroitan sulfate, inhibited the transduction. In addition, adenovirus containing a FLAG epitope in the fiber protein was used to target the FcR expressed on B cells using an anti-FLAG antibody. In the presence of anti-FLAG, the modified adenovirus was able to efficiently transduce LPS-activated B cells and several B cell lymphoma lines. Interestingly, in the absence of anti-FLAG, there was low level transduction in the LPS-blasts and in M12.4.1 that was not inhibited by soluble adenovirus fiber protein or agents that block RGD-integrin interactions. These results demonstrate that modified adenovirus efficiently transduce B lymphocytes which will be critical for targeting genes to normal or malignant B cells.
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PMID:Efficient transduction of murine B lymphocytes and B lymphoma lines by modified adenoviral vectors: enhancement via targeting to FcR and heparan-containing proteins. 1142 34


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