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

Report of a T-cell rich B-cell lymphoma (TCRBCL) in a 43 years old man with an associated haemophagocytic syndrome (HS). At presentation the haemophagocytic cells involved the same organs as the lymphoma, i.e. spleen, liver, abdominal lymph nodes and bone marrow. As supportive measure to alleviate chemotherapy-induced granulocytopenia the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) was given. After an initial improvement of the blood granulocyte count pancytopenia developed again, resulting in fatal sepsis. Autopsy demonstrated massive proliferation of macrophages in the bone marrow with haemophagocytosis as morphological correlation to the pancytopenia. The observation that exogenous GM-CSF enhanced the preexistent HS primarily reactive to the TCRBCL raises the question if endogenous GM-CSF may play a role in triggering a HS. The observed association of TCRBCL and HS has not been reported so far.
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PMID:[T-cell rich B-cell lymphoma associated with hemophagocytic syndrome]. 128 41

We investigated the anti-tumor effects of recombinant mouse interleukin (IL)-4 and IL-5 by using a transplantable B cell lymphoma 38C13 cell line as a model. Daily local administration of either IL-4 or IL-5 produced moderate but significant inhibition of the rate of local tumor growth and prolongation of mean survival time (MST) in syngeneic C3H/HeJ mice; these anti-tumor effects appeared to plateau at low doses. Histopathologic and immuno-histochemical examination revealed necrotic changes in the cytokine-treated tumors, associated with infiltration of inflammatory cells such as eosinophils, macrophages, and lymphocytes. The infiltrating lymphocytes were found to be Thy-1.2+ T cells. To elucidate the importance of T cells, the rate of tumor growth and the MSTs were compared between athymic T cell-deficient BALB/c nude mice and immunocompetent C3H/HeJ mice. In the nude mice the transplanted tumor grew more rapidly and the MST was shorter than in the normal mice, suggesting a significant contribution of infiltrating T cells in the anti-tumor effects of the interleukins. Lastly, in vitro, growth inhibition of the 38C13 cells was observed in a dose-dependent manner at relatively high concentrations of either cytokine. Therefore, we conclude that both IL-4 and IL-5 have moderate anti-tumor effects against 38C13 B cell lymphoma both in vivo and in vitro, and that the observed in vivo anti-tumor effects are probably mediated both by tumoristatic action of infiltrating cells, such as eosinophils, macrophages and T lymphocytes, and by direct anti-proliferative action of the recombinant cytokines.
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PMID:Anti-tumor effects of interleukin-4 and interleukin-5 against mouse B cell lymphoma and possible mechanisms of their action. 155 1

C.B-17 severe combined immune deficient (SCID) mice, which lack functional B and T lymphocytes, allow xenografts and, therefore, can be used to study the biology of human malignancies. Two different human B cell lymphoma cell lines, SU-DHL-4 and OCI-Ly8, which both harbor the t(14;18) chromosomal translocation, were injected into C.B-17 SCID mice. Mice injected intravenously or intraperitoneally developed tumors and died in a dose-dependent manner. The presence of tumor cells in various murine tissues could be demonstrated by a clonogenic tumor assay, staining of frozen sections with a monoclonal antibody (mAb) against a human B cell antigen (CD19), and with the polymerase chain reaction technique. A protocol using cytotoxic effector cells was developed and used to selectively deplete the tumor cells from bone marrow. These cells were developed by growing peripheral blood mononuclear cells in the presence of interferon gamma (IFN-gamma), anti-CD3 mAb, and interleukin 2 (IL-2). The timing of IFN-gamma treatment was critical and optimal if IFN-gamma was added before IL-2 treatment. The cells that were stimulated by IFN-gamma, followed by IL-2, could be expanded by treatment with a mAb directed against CD3. These cells could be further activated by IL-1, but not by tumor necrosis factor alpha. With this protocol, a tumor cell kill of 3 logs was obtained as measured by a clonogenic assay. Interestingly, despite their high cytotoxic activity against lymphoma cells, these cells had little toxicity against a subset of normal human hematopoietic precursor cells (granulocyte/macrophage colony-forming units). These cells were further tested by treating murine bone marrow contaminated with the human lymphoma cell line SU-DHL-4, and injecting these cells into SCID mice to assay for tumor growth in vivo. The animals injected with bone marrow contaminated with SU-DHL-4 cells had enhanced survival if the bone marrow was treated with the cytokine-induced killer cells before infusion. The SCID mouse provides a useful in vivo model for evaluation of new therapeutic approaches for lymphoma treatment. The cytokine-induced killer cells generated as described here could have an important impact on bone marrow purging for autologous bone marrow transplantation as well as for adoptive immunotherapy.
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PMID:Use of a SCID mouse/human lymphoma model to evaluate cytokine-induced killer cells with potent antitumor cell activity. 171 60

We identified a new cytokine, B cell-derived T cell growth factor (B-TCGF), that is produced by a murine B cell lymphoma and induces proliferation of mature and immature thymocytes in the presence of IL-2 and IL-4. Both adult and day 15 fetal thymocytes (CD4-8-, CD4+8-, CD4-8+) proliferate strongly in the presence of IL-2, IL-4, and B-TCGF. B-TCGF alone does not stimulate thymocyte proliferation. B-TCGF appears to be identical to a novel cytokine whose cDNA was recently isolated at our institution, cytokine synthesis-inhibitory factor (CSIF; IL-10). rIL-10 has B-TCGF activity, and mAb specific for IL-10 inhibit the B-TCGF activity present in CH12 supernatants. Further studies have shown that day 15 fetal thymocytes cultured in the presence of IL-10, IL-2, and IL-4 remain CD4- and CD8- but exhibit increased CD3 expression. Adult CD4- CD8- thymocytes cultured under the same conditions proliferate whether they are CD3+ or CD3-. The CD3- population becomes enriched in CD3+ cells after 4 days of culture. IL-10 is secreted by day 15 fetal thymocytes, adult thymocytes, and adult splenocytes when stimulated via their TCR. IL-10 is strongly homologous to the EBV gene BCRFI, and BCRFI has CSIF activity. In contrast to IL-10, BCRFI does not exhibit detectable thymocyte-stimulating activity, suggesting the existence of at least two functional epitopes on the IL-10 molecule.
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PMID:IL-10, a novel growth cofactor for mature and immature T cells. 212 36

We have utilized cultured Langerhans cells to activate and expand hapten- and protein-specific T-helper cells from nonsensitized mice. The generation of these lines was strongly dependent on eliminating all autologously reacting cells from the responder T-cell population. Primary in vitro sensitization was not uniquely induced with cultured Langerhans cells as splenic dendritic cells could subserve the same function. Despite its ability to induce strong allogeneic T-cell responses as well as hapten-specific secondary responses, M12c cells, a class II-bearing B-cell lymphoma line, could not activate hapten-specific T-helper cells in vitro. After primary or secondary in vitro stimulation, the T-helper cells which are generated secrete IL-2 and are able to adoptively transfer hapten-specific contact sensitivity, thus stimulating Type-1 T-helper cells. The T-helper cell lines which were generated after repeated cycles of stimulation stimulated type-2 T-helper cells in that they produced IL-4 and depended on this cytokine for autocrine growth. As well, when cultured with syngeneic, hapten-modified, small resting B cells, these T-helper cells caused specific IgE production. Thus, the studies reported herein demonstrate that it is possible to activate and expand T-helper cells with desired specificity from nonsensitized animals in vitro. Previous studies have demonstrated that expansion and adoptive transfer of effector T cells with specificity for tumor-associated antigens may be useful in the control of certain tumors; T-helper cells generated by in vitro sensitization should also be useful in adoptive immunotherapy.
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PMID:Generation and characterization of T-helper cells by primary in vitro sensitization using Langerhans cells. 214 19

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

Twenty-one cases of large, B-cell lymphoma with an unusually high content of reactive T lymphocytes are described in this report. Fifteen patients presented with lymphoma in nodal sites and six patients presented with lymphoma in extranodal sites. With two exceptions, all patients were more than 50 years of age. The male to female ratio was 1:2. Histologically, isolated to small groups of large lymphoid cells were intermingled with many small lymphocytes. The large cells were neoplastic and exhibited B-lineage markers; immunoglobulin light chain restriction could be demonstrated in two thirds of the cases. There was a rich infiltrate of immunophenotypically mature T lymphocytes that comprised more than 50% of the cellular population. The T lymphocytes ranged from small cells with dark, round nuclei to slightly larger cells with elongated, irregular nuclei. There were occasional medium-sized blastic cells. There was also a variable infiltrate of histiocytes with or without epithelioid features, eosinophils and plasma cells, and increased vascularity. The peculiar morphologic features were also reproduced in other sites in the four patients for whom additional histologic materials were available for examination. We postulate that the abundance of T cells results either from a florid host reaction or from cytokine secretion by the neoplastic B cells, attracting T cells to the vicinity. The morphologic and immunologic features mimic those of a variety of benign lymphoproliferative diseases, angioimmunoblastic lymphadenopathy and lymphomas arising in angioimmunoblastic lymphadenopathy, peripheral T-cell lymphoma, secondary B-immunoblastic lymphoma, and Hodgkin's disease. Careful morphologic evaluation and immunophenotypic studies using leukocyte antibodies reactive in paraffin-embedded sections are of great assistance in determining a diagnosis.
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PMID:Large B-cell lymphomas with a high content of reactive T cells. 259 44

A B-cell lymphoma cell line, designated KML-1, was established from pleural effusion of a patient with non-Hodgkin's lymphoma of large-cell type. The lymphoma arose in the pelvis and ran an aggressive clinical course. Chromosome analysis of the cell line exhibited a complex karyotype including the loss of chromosome 18. To evaluate the molecular events in the cell line that may be associated with the development of the lymphoma, we investigated the expression and/or alterations of several classes of human genes, including oncogenes, tumor suppressor genes, and cytokine genes. The expression of the DCC (deleted in colorectal cancer) gene, located on the chromosome 18q21, was extremely reduced in KML-1 cell line, as compared with that in a normal spleen tissue and other 4 lymphoma cell lines by the reverse transcription-polymerase-chain-reaction (RT-PCR) method. This finding suggests that inactivation of the DCC gene might play a role in the pathogenesis of the case of lymphoma.
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PMID:Inactivation of the DCC tumor suppressor gene in a B-cell lymphoma cell line with the alteration of chromosome 18. 757 91

The high incidence of spontaneous T cell lymphomas in AKR mice (affected by sustained viremia) can be greatly reduced by experimental manipulations including thymus removal at young age or by genetic manipulation changing the Fv-1 allele that controls replication and spread of viruses (establishing the congenic AKR.Fv-1b mice). Although T cell lymphomagenesis is prevented, all these mice were shown to carry endogenous ecotropic provirus-induced potential lymphoma cells (PLCs) in a dormant state. The termination of the dormant state, leading to a high incidence of CD5+ IgM+ B cell lymphomas, was triggered by interference with T cell functions (optimal effect observed following in vivo administration of anti-CD8 moAb), administration of T cell growth factors or by injecting the MCF-247 recombinant virus isolate (from AKR origin) that affects T cell functions. The assumption that the PLC dormant state is maintained through specific immunological mechanisms (involving T cells or antibodies recognizing PLCs) could not be substantiated experimentally. The results of the present studies suggest that T cells provide immunoregulatory signals or factors that contribute to the maintenance of the B cell lymphoma arrest and/or proliferation. Analysis of cytokine levels produced by splenocytes taken from mice during PLC dormancy or its breakdown indicated reduced levels of IL-2 and IL-4 and marked elevation of IL-1 and IL-6 associated with the termination of the dormant state. The effect of IL-1 and IL-6 on terminating the dormant state was demonstrated by injecting these cytokines into PLC carriers, thymectomized 12-month-old AKR mice, yielding 80-85% CD5+ IgM+ B cell lymphomas. The role of IL-6 on B cell lymphoma proliferation was also indicated in MCF-247 mediated termination of dormancy, by inhibiting significantly its effect via in vivo administration of anti IL-6 moAbs.
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PMID:Role of cytokines in termination of the B cell lymphoma dormant state in AKR mice. 759 76

We have examined the antitumor activity of murine interleukin 4 (IL-4) on development of a human B-cell lymphoma (Daudi) in severe combined immunodeficient (SCID) mice. The progression of Daudi cells in SCID mice was followed by histological staining and by flow cytometric analysis of CD20+ cells in spleen, liver, bone marrow, and kidneys. By day 35, CD20+ Daudi cells populate the majority of space in the bone marrow and kidney in vehicle-treated mice. Mice receiving i.p. injections of IL-4, commencing 7 or 14 days after tumor inoculation, exhibit a reduction in tumor burden as well as a decrease in CD20+ cells in both compartments. The antitumor activity of IL-4 does not appear to be due to an antiproliferative effect, since the cytokine does not alter the growth of Daudi cells in vitro, nor does it correlate with any marked cellular infiltrate in tumor-bearing tissues. In 51Cr-release assays, we observed that splenocytes from IL-4-treated mice were capable of lysing YAC-1 but not Daudi cell targets. Our findings demonstrate that: (a) systemic administration of IL-4 retards dissemination of a human B-cell lymphoma in SCID mice; and (b) antitumor activity elicited by IL-4 may not involve a direct effect on proliferation of Daudi cells or on the induction of cytolytic activity.
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PMID:Interleukin 4 retards dissemination of a human B-cell lymphoma in severe combined immunodeficient mice. 764 Nov 77


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