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

Three predominantly CD8+ CTL lines, TIL 501, TIL 620, and TIL 660, were generated from three HLA-A2+ melanoma patients by culturing tumor-infiltrating lymphocytes in 1000 U/ml IL-2. These tumor-infiltrating lymphocytes lysed 12 of 18 HLA-A2+ autologous and allogeneic melanomas, but none of 20 HLA-A2-negative melanomas. They also did not lyse the MHC class I negative lymphoma-leukemia cell lines, Daudi, K562, or HLA-A2+ non-melanoma cell lines including PHA or Con A-induced lymphoblast, fibroblast, EBV-transformed B cell, Burkitt's B cell lymphoma, and colon cancer cell lines. Autologous and allogeneic melanoma lysis was inhibited by anti-CD3, by anti-MHC class I, and by anti-HLA-A2 mAb, indicating recognition of shared tumor Ag among melanoma cell lines in a TCR-dependent, HLA-A2-restricted manner. Six HLA-A2-negative melanoma cell lines obtained from five HLA-A2-negative patients were co-transfected with the HLA-A2.1 gene and pSV2neo. All 17 cloned transfectants expressing cell surface HLA-A2 molecules, but none of 12 transfectants lacking HLA-A2 expression, were lysed by these three HLA-A2-restricted, melanoma-specific CTL. Lysis of the HLA-A2+ transfectants was inhibited by anti-CD3, by anti-MHC class I, and by anti-HLA-A2 mAb, indicating recognition of shared tumor Ag on transfectants in a TCR-dependent, HLA-A2-restricted manner. These results identify the HLA-A2.1 molecule as an Ag-presenting molecule for melanoma Ag. They also suggest that common melanoma Ag are expressed among melanoma patients regardless of HLA type. These findings have implications for the development of melanoma vaccines that would induce antitumor T cell responses.
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PMID:Shared human melanoma antigens. Recognition by tumor-infiltrating lymphocytes in HLA-A2.1-transfected melanomas. 172 79

Using a newly established HTLV-1 positive T cell line as an immunogen, a new monoclonal antibody, Ber-ACT8, was produced. It reacts with in vitro activated T cells and a small subset of normal resting T cells, but not with resting B cells or any of the 29 established human permanent cell lines tested. Immunohistological analysis of a wide spectrum of human tissues showed that Ber-ACT8 reactivity is restricted to a few T cells in the peripheral blood, the extrafollicular areas of lymph nodes and tonsils, and splenic red pulp. In the gut Ber-ACT8 labelled most intraepithelial T cells and up to 50% of lamina propria T cells. The antibody also immunostained T cells present in the oral and bronchial mucosa. Double labelling on splenic cells, fresh blood lymphocytes, and in vitro activated T cells showed that most Ber-ACT8 positive cells coexpressed CD8. Ber-ACT8 did not react with any of the 14 Hodgkin's lymphomas nor any of the 172 non-Hodgkin's lymphomas tested, with the exception of 10 cases of T cell lymphomas, five of which were located in the jejunum and associated with coeliac disease, and one B cell lymphoma, and most cases of hairy cell leukaemia tested. Parallel immunostainings with Ber-ACT8, anti-TCR-beta (beta F1), and anti-TCR-delta showed that most Ber-ACT8 positive T cells carry the TCR of alpha beta type. Comparison of Ber-ACT8 with HML-1, B-ly7, and LF61 showed essentially the same reactivity and an identical molecular target. The molecular structure recognised seems to be a trimeric molecule with components of 150, 125 and 105 kilodaltons, with the Ber-ACT8 epitope localised on the 150 kilodalton chain. The 150 kilodalton molecule contains an 0-linked carbohydrate moiety of about 10 kilodaltons. Because of its very selective distribution, the trimeric antigen is a powerful reagent for the diagnosis of gut T cell-derived T cell lymphomas and other extranodal T cell lymphomas, as well as hairy cell leukaemia.
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PMID:Ber-ACT8: new monoclonal antibody to the mucosa lymphocyte antigen. 189 Jan 96

We have compared the functional properties of I-Ad expressed on different cell types. Specifically, we have transfected I-A alpha d and I-A beta d cDNA into a panel of T cell thymomas of various phenotypes. Excellent class II surface expression was achieved in all T cell tumors, equivalent in level to that found on the B cell lymphoma A20. Interestingly, however, two allo-I-Ad-specific Thy differed in their recognition of the transfected tumor cells: whereas the 42H11 T cell hybridoma (THy) was stimulated very efficiently by all transfectants, the RK38.2.2 Thy did not react to any of them. Both THy responded equally well to I-Ad on A20 B lymphoma cells. Purified macrophages isolated from various sources were also differentially recognized by the two THy, although there was only a quantitative difference in stimulation. Taken together, these results are best interpreted to show that the TCR of the RK38.2.2 THy is specific for I-Ad in the context of a B cell-specific determinant, possibly a self-peptide that is naturally associated with Ia. A cross-reactive molecule could be expressed by macrophages and COS-1 cells, but not by T cells.
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PMID:The expression of a tissue-specific self-peptide is required for allo-recognition. 196 23

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

Numerous chromosome abnormalities are repeatedly found in the acute leukemias. These abnormalities have both diagnostic and prognostic utility. Some abnormalities, such as the t(4;11) (q21;q23) and t(9;22) (q34;q11) are found in both lymphoid and myeloid leukemias. In both disorders, these rearrangements are associated with a poor prognosis. Some abnormalities are found exclusively in myeloid malignancies, e.g., the t(8;21) (q22;q22) and rearrangements of chromosome 16q22, both of which carry a good prognosis. Other abnormalities are found only in lymphoid malignancies, like those of chromosome 14 at band q11 which involve T lymphoblasts. T-cell receptor (TRC) genes have been mapped to the 14q11 band. Recombinations involving the TCR alpha gene and the myc oncogene have been found in the t(8;14) (q24;q11). Similar involvement of immunoglobulin heavy chain genes and the myc oncogene has been well documented in molecular studies of B-cell lymphoma patients with a t(8;14) (q24;q32).
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PMID:Clinical significance of the cytogenetics of acute leukemias. 214 23

To investigate bovine leukemia virus (BLV)-induced leukemogenesis, we infected sheep with BLV and used flow-cytometric and immunohistological analysis to characterize the phenotypic alterations in lymphocytes from peripheral blood and lymph nodes taken from the animals with lymphoma at various stages. In sheep at the asymptomatic stage, depending on the extent of progression of the disease, the proportions of CD2(+)-, CD4(+)-, CD8(+)-, and gamma delta TCR(+)-T cells that coexpressed CD5 decreased, but CD5+ sIgM+ cells as well as CD5- sIgM+ cells increased for a period. The number of CD5+ B cells, however, rapidly decreased in the lymphoma stage. On the other hand, neoplastic lymphocytes appeared to be a monoclonal population derived from a single cell with surface phenotypes of sIgM+, B-cell-specific molecule B2+, major histocompatibility complex (MHC) class II+, OvCD5-, OvCD2-, OvCD4-, OvCD8-, gamma delta TCR-, which suggests that only CD5- B cells proliferate clonally when the disease proceeds to the lymphoma stage. Thus, rapid decrease of CD5+ B cells may be used as a marker of lymphoma stage. To identify the BLV provirus in the CD5- B and CD5+ B cells throughout the course of disease, each fraction of CD5- B and CD5+ B cell was sorted from the peripheral blood by flow cytometry and nested double polymerase chain reaction was performed. In BLV-infected but healthy sheep, BLV integrated both CD5- B and CD5+ B cells. In lymphoma, however, BLV provirus was detected only in CD5- B cells but not in CD5+ B cells. Therefore it appears that a disappearance of BLV-infected CD5+ cells is one of the critical events leading to CD5- B cell lymphoma in sheep. This is in contrast to the BLV-induced lymphoma in cattle which shows CD5+ phenotype.
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PMID:Bovine leukemia virus induces CD5- B cell lymphoma in sheep despite temporarily increasing CD5+ B cells in asymptomatic stage. 751 99

A case of T cell-rich B cell lymphoma (TCRBCL) with Epstein-Barr virus (EBV) infection in tumor cells is reported. A 50 year old male developed right cervical lymph node swelling in July 1988. Initial biopsy in April 1989 demonstrated many scattered Hodgkinoid atypical cells with Lennert's lesion. After partial remission following chemotherapy, the lymph nodes enlarged again, and a second biopsy in February 1991 showed an IBL-T-like lesion. Only a small number of Hodgkinoid atypical cells were still observed. After apparently, complete remission, the lesion soon recurred and the patient died in November 1992. Immunohistochemically the Hodgkinoid cells were positive for L26, but negative for LN2, LN3, UCHL-1, MT1, lysozyme, Ber-H2 and Leu-M1. Reactivity for immunoglobulins showed false-positive because of polyclonal staining. IgH monoclonality was detected by the polymerase chain reaction method in the first biopsied specimen, and by Southern blotting in the second biopsied snap-frozen specimen. Monoclonal TCR beta rearrangement was not detected. The Hodgkinoid atypical cells were positive for EBV-encoding RNA by in situ hybridization, and LMP-1 by immunostaining. Occasionally, EBV-bearing immunoblastic, medium sized, or small lymphocytic cells were also observed. This case indicates the possibility that EBV is related to the pathogenesis of TCRBCL.
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PMID:T cell-rich B cell lymphoma bearing Epstein-Barr virus in tumor cells: a case of IBL-T-like lesion following Lennert's lesion. 758 39

Autoptic findings of a 77-year-old man with T-cell-rich B-cell lymphoma (TCRBCL) showed predominant infiltration of reactive T-cells with a minority population of neoplastic B-cells in liver, spleen, pancreas, adrenal gland, stomach, small intestine and heart, as well as, lymph node. DNA studies demonstrated dual rearrangement in the T-cell receptor beta (TCR beta), immunoglobulin heavy chain J region (IgJH) and kappa light chain J region (IgJ kappa) genes.
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PMID:An autopsied case of T-cell rich B-cell lymphoma with general involvement. 760 90

A 76-year-old man visited our clinic with chest radiographic evidence of a coin lesion in the right middle lung. Chest CT demonstrated an infiltrative shadow mainly in the S4 segment. Lymphoproliferative disorders were suggested by transbronchial lung biopsy. Middle lobectomy was performed. Pathological study showed massive proliferation of mature lymphocytes. Immunoperoxidase studies could not demonstrate a neoplastic monoclonal process. Pseudolymphoma was diagnosed. High molecular weight DNAs were extracted from frozen specimens. Whether genes of immunoglobulins and T-cell receptors were rearranged was investigated using DNA probes against JH and TCR beta-1 receptor gene. One rearranged band was found in the JH chain. No rearranged band appeared in TCR beta-1 chain. B cell lymphoma was diagnosed instead of pseudolymphoma.
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PMID:[A case of primary pulmonary B cell lymphoma confirmed by gene analysis]. 766 57

H-2b mice are immunologic responders to the tumorigenic MCF1233 murine leukemia virus (MuLV), an AKV-related virus derived from endogenous C57BL MuLV. We have identified an immunodominant CTL epitope that is expressed on MCF1233 MuLV-induced lymphomas of H-2b mice. C57BL/10 (B10) mice were immunized with an MCF1233-induced B10 B cell lymphoma, and tumor-specific CTL cultures were generated in vitro. These were tested for recognition of synthetic class I-binding MuLV peptides, selected for class I allele-specific motifs. One of 28 candidate peptides sensitized target cells for CTL recognition. This peptide seems to be an immuno-dominant epitope, because it was recognized by all independent CTL clones, isolated from the tumor-specific bulk culture. The epitope (KSPWFTTL) is derived from the MCF1233 MuLV envelope (env)-p15E region and is shared by all endogenous AKV types of MuLV. It has an optimal length of eight amino acids and is presented by the Kb H-2 class I molecule. Interestingly, Friend, Moloney, and Rauscher (FMR) types of MuLV are not recognized by MCF MuLV-directed CTL. The FMR env-p15E proteins have a single amino acid difference at the first position of the MCF1233 MuLV epitope (RSPWFTTL instead of KSPWFTTL). The corresponding FMR-encoded peptide bound class I H-2 Kb equally well as the MCF peptide, but it was poorly recognized by MCF1233 MuLV-specific CTL. Moreover, in the Rauscher MuLV-induced cell line RMA the FMr peptide seems not to be processed for recognition by CTL, which was illustrated by experiments with CTL elicited against this peptide. Altered TCR interaction as well as lack of processing thus may explain the type specificity of MCF1233 MuLV-directed CTL.
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PMID:Immunodominant mink cell focus-inducing murine leukemia virus (MuLV)-encoded CTL epitope, identified by its MHC class I-binding motif, explains MuLV-type specificity of MCF-directed cytotoxic T lymphocytes. 825 84


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