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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of interferon (IFN) and tumour necrosis factor (TNF), either alone or combined with hyperthermia, on cell proliferation and expression of idiotype antigen on a murine B-cell lymphoma has been studied. Incubation with same doses of IFN-alpha and IFN-gamma reduced cell proliferation to the same extent. Hyperthermia potentiated the antiproliferative activity of IFN-alpha and IFN-gamma. Pretreatment with IFN-gamma induced a synergistic response with heat, while IFN-alpha and heat had an additive effect. Tumour necrosis factor (TNF) alone did not affect cell proliferation, nor did TNF modify the heat-induced delay in cell growth. The quantitative expression of surface idiotype antigen was studied by flow cytometry using an anti-idiotype monoclonal antibody (MAb). Heat reduced the expression of idiotype antigen approximately 50%. The duration of the reduction depended on the heat-dose. Recovery of antigen expression correlated with recovery of cell growth, and 2-5 days after the treatment antigen expression returned to the normal level for untreated cells. IFN-gamma and TNF increased antigen expression (30-50%) which lasted for 4-6 days after treatment. When cells were incubated with IFN-gamma or TNF for 2 days prior to hyperthermia, the increase in antigen expression was observed immediately after heating, but by the following day, antigen expression was similar to that after heat treatment alone. Expression of idiotype antigen recovered within 2-5 days to the same values as after heat treatment alone. IFN-alpha alone or combined with hyperthermia did not have any significant effect on antigen expression.
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PMID:Changes in the expression of idiotype antigen on murine B-cell lymphoma after hyperthermia alone and in combination with interferon and tumour necrosis factor. 168 4

The Ly-6 family of cell surface molecules has previously been shown to participate in T cell activation. We show that Ly-6A/E proteins also modulated the response of normal B lymphocytes in three separate in vitro assays. First, unfractionated or small resting B cells proliferated when cultured with IFN-gamma, IL-4, and an anti-Ly-6A/E mAb. Second, this anti-Ly-6A/E mAb restored B cell proliferation responses that were inhibited when coculturing the B cells in IFN-gamma, IL-4, and anti-IgM. Third, anti-Ly-6A/E specifically up-regulated the cell surface expression of its own Ag, and this response was dependent upon co-stimulation with IFN-gamma. Mixing of T and B cells in culture suggested that T cells did not contribute substantially to the B cell proliferative response. Moreover, up-regulation of Ly-6A/E was observed for one B cell lymphoma, WEHI-231. Therefore, it appeared that modulation of B cell function by anti-Ly-6A/E was due to a direct effect of the mAb binding to the B cells. Taken together, these data suggest Ly-6A/E proteins are functional on B cells and may play a regulatory role in B cell activation.
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PMID:Regulation of B lymphocyte responses to IL-4 and IFN-gamma by activation through Ly-6A/E molecules. 210 54

Although the MHC class II genes are known to be regulated transcriptionally, the relative rates of transcription of the four classical class II genes in different cell types have not been investigated. Using nuclear transcriptional analysis, we have investigated the transcriptional rates of the class II genes in the macrophage cell line WEHI-3, normal bone marrow-derived macrophages, L-929 cells, and two different B cell lymphoma lines. Kinetic analysis of class II transcription in IFN-gamma-treated WEHI-3 cells revealed a 4-h delay, followed by a rapid increase in transcription over the next 20 h. A significant basal level of class II transcription, apparent in bone marrow derived macrophages, was also further enhanced by IFN-gamma treatment. None of the class II genes were transcribed in L cells, whereas all class II genes were transcribed constitutively in the B cell lines. In both B cell lines and macrophages, the four class II genes were found to be transcribed at different rates from one another, but the only gene showing a consistent pattern in multiple experiments was A-alpha, always showing the highest rate. We also investigated the effect of protein synthesis inhibition on class II transcription. Cycloheximide treatment of WEHI-3 cells did not inhibit IFN-gamma-induced transcription of the class II genes within 8 h, suggesting that IFN-gamma acts on pre-existing trans-acting factors, rather than inducing their synthesis. In contrast, treatment of B cells with cycloheximide for 8 h significantly reduced class II transcription, suggesting that, in B cells, continuous synthesis of a labile trans-acting factor is required for constitutive expression. These data support the notion that class II expression in B cells is mediated by trans-acting factors distinct from those found in macrophages.
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PMID:MHC class II transcription in different mouse cell types. Differential requirement for protein synthesis between B cells and macrophages. 249 89

Mouse class II major histocompatibility complex genes have been shown to be regulated at the level of transcription for both tissue-specific and inducible expression. In particular, IFN-gamma induction of the class II genes has been shown to occur at the transcriptional level, although the role that additional post-transcriptional mechanisms of regulation may play in this induction is not known. To evaluate IFN-gamma effects on transcriptional and post-transcriptional events of class II gene expression, we examined the rate of decline of class II transcription, steady-state mRNA, and cell surface protein following the removal of IFN-gamma from maximally stimulated WEHI-3 cells (an IFN-gamma inducible, myelomonocytic cell line). We determined that transcription of class II genes almost completely returned to baseline levels eight hours after removal of IFN-gamma. However, the steady-state level of class II mRNA's required 4 days, and membrane Ia expression required 5 days to return to baseline levels. This decay was linear and allowed us to determine a half-life value of 16-20 h for class II transcripts. These data demonstrate that, following removal of IFN-gamma from fully stimulated cells, transcription of the class II genes declined rapidly, but mRNA was quite long-lived. We also assessed the class II mRNA stability in unstimulated WEHI-3 cells and the B-cell lymphoma. A20/2J, by actinomycin D treatment and northern blot analysis. In agreement with the IFN-gamma washout experiments, transcripts from all four class II genes were quite long-lived in these cell types, with a half-life greater than ten hours. These data support the concept that IFN-gamma acts primarily at the level of class II transcription and argues against IFN-gamma playing a major role in post-transcriptional modulation of class II expression.
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PMID:Evidence that IFN-gamma does not affect MHC class II gene expression at the post-transcriptional level in a mouse macrophage cell line. 250 46

We previously showed that cloned, antigen-specific, Ia-restricted L3T4a+ T cell lines can be cytolytic for antigen-pulsed B cell lymphoma targets. Such cells can also, under different experimental conditions, activate B cells to proliferate and secrete immunoglobulin. In the present experiments, we show that this functional phenotype is a common one among a panel of cloned T cell lines. In keeping with this finding, freshly isolated, antigen-activated lymph node T cells show similar functional properties. Such cytolytic L3T4a+ T cells differ from classical H-2K/D-restricted cytolytic T cells in two distinct ways. First, Ia-restricted cytolytic T cells can kill bystander targets, whereas H-2K/D-specific cytolytic T cells do not. Second, in testing a panel of target cells by using lectin-mediated cytolysis, Ia-restricted cytolytic clones reveal large differences in target cell susceptibility, whereas all targets are similarly susceptible to H-2K/D-specific killer cells. Finally, evidence is presented that both direct and bystander killing effected by L3T4a+ T cells are mediated by the same soluble factors, in that there is a strong positive correlation of these two activities for individual cloned lines. The relevant mediators appear to be lymphotoxin and IFN-gamma, although the latter molecule by itself is not cytolytic on our target lines.
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PMID:Protein-antigen specific Ia-restricted cytolytic T cells: analysis of frequency, target cell susceptibility, and mechanism of cytolysis. 258 34

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

The murine B cell lymphoma, 70Z/3, serves as a model for the L chain activation seen when normal B cells develop from pre-B into B cells. 70Z/3 cells can be induced to activate transcription of their endogenous kappa L chain by exposure to exogenous factors in vitro, such as LPS and IFN-gamma. In order to study the interaction of transacting factors with sequences of the kappa gene responsible for their activation, altered kappa genes could be introduced into 70Z/3 cells and their induction patterns studied. As a preliminary step to such studies, we show that wild-type kappa genes stably integrated into 70Z/3 cells can be expressed normally and that their pattern of induction by LPS and IFN-gamma is indistinguishable from wild-type 70Z/3 cells. By using electroporation, gamma genes were co-transfected with either the neo or gpt selectable genes. In all cases, the expression of the kappa genes was autonomous, reflecting neither regulation by the selected markers nor by flanking chromosome sequences. A noninducible variant of 70Z/3, NN12, also increased mRNA levels from transfected kappa genes in response to LPS and IFN-gamma, suggesting that its defect is in its endogenous kappa gene. These results demonstrated the usefulness of this approach for distinguishing between variants that have structural defects in their endogenous kappa gene from variants that have defects in transacting factors or other steps in the induction pathways.
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PMID:Inducible expression of transfected kappa light chains by lipopolysaccharide and IFN-gamma in the murine B lymphoma, 70Z/3. 312 55

T cell-replacing factor (TRF)/IL-5 is a glycosylated polypeptide that acts as a key factor for B cell growth and differentiation. Since IL-5 action is probably mediated by specific cell surface receptor(s), we have characterized the binding of IL-5 to cells using biosynthetically [35S]methionine-labeled IL-5 and 125I-IL-5 that had been prepared using Bolton-Hunter reagent. The radiolabeled IL-5 binds specifically to BCL1-B20 (in vitro line) (a murine chronic B cell leukemic cell line previously shown to differentiate into IgM-secreting cells in response to IL-5) within 10 min at 37 degrees C. There are two classes of binding sites with high affinity (Kd = 66 pM) and low affinity (Kd = 12 nM) for IL-5 and an average number of binding sites for high affinity and for low affinity were 400 and 7,500 per cell, respectively. The specificity of binding of radiolabeled IL-5 has been confirmed by demonstrating that only unlabeled IL-5 and anti-IL-5 mAb but not by IL-1, IL-2, IL-3, IFN-gamma, and GM-CSF inhibit radiolabeled IL-5 binding to BCL1-B20 cells. Treatment of surface-bound radiolabeled IL-5 with bivalent crosslinkers identified a membrane polypeptide of Mr 46,500 to which IL-5 is crosslinked. A variety of cell types have been surveyed for the capacity to bind specifically radiolabeled IL-5 with high affinity. BCL1 cells MOPC104E (murine myeloma cell line) expressed IL-5-R, whereas BAL. 17 and L10 A (B cell lymphoma) did not. T cell line, mastocytoma cell line, or macrophage tumor cell line did not display detectable levels of IL-5-R. were hardly detectable on normal resting B cells but were expressed on LPS-activated B cells, fitting the function of IL-5 that acts on activated B cells for their differentiation into Ig-secreting cells. Intriguingly, early B cell lines (J-87 and T-88) that grow in the presence of IL-5 expressed significant but low numbers of high-affinity binding sites for IL-5. The biological effects of IL-5 were mediated by high-affinity binding sites. The identification and characterization of IL-5-R should provide new insight into the apparent diverse biological activities of IL-5.
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PMID:Receptors for T cell-replacing factor/interleukin 5. Specificity, quantitation, and its implication. 326 7

Human mononuclear leukocytes (MNL) produced several factors with fibroblast proliferation activity (FPA) for HFL-1, a human lung fibroblast cell line, when MNL were cocultured with irradiated BALL-1, a B cell lymphoma line (BCLL), but not with other BCLL. The cellular source of BALL-1-induced FPA seemed to be CD4-positive T lymphocytes. On isoelectric electrophoresis, major activity of BALL-1-induced FPA was detected in the fractions around pH 4-5, and minor activity was present in the fractions around pH 6-7. Major BALL-1-induced FPA consisted of at least 4 different fibroblast proliferation factors (FPFs) according to their molecular weight; 320-600 kDa (P-I), 50-110 kDa (P-II), 22-38 kDa (P-III) and 4.6-11 kDa (P-IV). P-I had affinity to heparin though the rest had little or no affinity. FPA of P-I was suppressed by an antibody against acidic FGF, and FPA of P-III was suppressed by an antibody against IL-6. On the other hand, FPA of P-II and P-IV was suppressed by none of the antibodies against cytokines with FPA, such as FGF, IL-4, IL-6, IFN-gamma, TGF-beta and TNF-alpha. It was thus suggested that P-I was acidic FGF, that P-III was IL-6, and that P-II and P-IV were different cytokines from those described above. Furthermore, it was found that P-II and P-IV failed to exhibit proliferation activity for human umbilical vein endothelial cells (HUVEC).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Production of fibroblast proliferative cytokines from T lymphocytes stimulated by a B cell lymphoma line and their functional heterogeneity. 800 51

Chronic antral gastritis following Helicobacter pylori (Hp) infection is characterized by a cellular inflammatory infiltrate whose cytokines may represent a host-dependent factor influencing the outcome of the infection. The pattern of cytokines produced by the immunologically active cells in the gastric antrum was analyzed at the mRNA level in antral biopsies from five Hp-infected patients with duodenal ulcer and three Hp-negative dyspeptic controls. T cell clones were generated from parallel antral biopsies of the same Hp-infected patients and assessed for reactivity to Hp Ags, cytokine profile, and effector functions. Antral biopsies from all Hp-infected patients showed IFN-gamma, TNF-alpha, and IL-12, but not IL-4, mRNA expression, whereas no cytokine mRNA signal was found in the mucosa of controls. A total of 24 out of the 163 CD4+ T cell clones (15%) derived from Hp-infected patients proliferated in response to a Hp lysate; 11 clones (46%) also reacted with Cag-A, 2 with Vac-A, and 1 with urease. Upon Ag stimulation, 20 out of the 24 Hp-reactive clones (83%) produced IFN-gamma, but not IL-4 or IL-5 (Th1-like), whereas 4 produced IFN-gamma, IL-4, and IL-5 (Th0-like). All Hp-specific clones secreted high levels of TNF-alpha. At low T:B cell ratio, Hp-specific clones expressed Ag-dependent helper function for B cell proliferation and Ig production, whereas at higher T:B cell ratios, 15 Th1 and 2 Th0 clones lysed Ag-pulsed autologous EBV-transformed B cells. Results provide evidence for Hp-specific Th1 effectors in the gastric antrum of Hp-infected patients, where they may play a role in the genesis of either peptic ulcer or Hp-associated gastric B cell lymphoma.
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PMID:T helper 1 effector cells specific for Helicobacter pylori in the gastric antrum of patients with peptic ulcer disease. 899 17


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