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)

Specific DNA probes for genes encoding immunoglobulins (Ig) and the T cell receptor (TCR) are useful diagnostic tools in lymphoproliferative disorders. Gene rearrangement analysis was carried out in 2 cases of conjunctival lymphoid lesions. A 36-year-old man (case 1) had a 1-year history of left conjunctival tumor. A biopsy was performed and histopathological findings showed diffuse proliferation of small lymphocytes, but monoclonality was not revealed by immunophenotypic analysis. A right conjunctival lesion developed and five months later a biopsy of the left conjunctiva was performed again. A frozen sample was analyzed and immunoglobulin heavy chain gene rearrangement was found. A 53-year-old woman (case 2) had a 6-month history of bilateral conjunctival tumor. The first biopsy did not reveal monoclonality immunophenotypically. A second biopsy with a frozen specimen was analyzed and immunoglobulin heavy chain gene rearrangement was found. We diagnosed these two cases as B-cell lymphoma. We discuss the clinical value of gene rearrangement analysis as a diagnostic method for lymphoproliferative disorders.
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PMID:[Gene rearrangement analysis of conjunctival malignant lymphomas]. 141 4

M protein from type 5 group A streptococci has been identified as a member of the family of polyclonal T cell activators termed superantigens because it preferentially stimulates T cells bearing specific V beta elements of the T cell receptor (TCR). In this study the molecular and cellular requirements for presentation of this protein to T cells were investigated. Only accessory cells (AC) expressing class II major histocompatibility complex (MHC) molecules were capable of supporting T cell activation in response to a 22 kDa fragment of M protein (pep M). Despite the need for class II elements, processing of pep M5 by the antigen-presenting cells (APC) was not required for T cell proliferation induced by pep M5. Fixation of APC by paraformaldehyde (PF) treatment impaired their ability to induce optimal T cell proliferation in response to pep M5 without significantly affecting interleukin (IL-2) production. In contrast, PF-fixation of cells from the B cell lymphoma line, Raji, did not affect their ability to present pep M5 to human T cells. Addition of rIL-1 and IL-6 to PF-treated APC restored pep M5-induced blastogenesis. Our data suggest that pep M5 directly associates with HLA class II molecules forming a complex that can induce IL-2 production but not optimal proliferation by T cells. Additional signals provided by the AC are required to trigger optimal T cell proliferation in response to this superantigen.
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PMID:Metabolically active antigen presenting cells are required for human T cell proliferation in response to the superantigen streptococcal M protein. 157 92

In this study, we demonstrated that some V beta 6+, CD4+, Mls-1a-specific T cell clones had cytolytic activity when stimulated with anti-T cell receptor(TcR)/CD3 monoclonal antibodies (mAb), but not with targets expressing Mls-1a, although they produced lymphokines (interleukin 2 and interferon-gamma) in response to both types of stimuli. To examine the possibility that lack of cytolysis resulted from expression of the Mls-1a antigen on merely a fraction of splenic B blasts, we (a) used the B cell lymphoma LBB.3.4.16 and (b) measured esterase secretion which is generally concurrent with cytotoxic T lymphocyte (CTL) activity. The B cell lymphoma maximally stimulated the T cell clone for interferon-gamma production when responding and stimulating cells were incubated at a 1:1 ratio, but it was never killed by the Mls-1a-specific T cell clone unless TcR/CD3-specific mAb were added. Furthermore, a fivefold excess of the Mls-1a B cell lymphoma did not induce any secretion of esterase, which was observed only in the presence of the TcR/CD3-specific mAb. Comparison of the reactivity of two Mls-1a-specific T cell hybridomas expressing the same TcR at similar surface density, revealed both quantitative and qualitative differences between CD3-specific mAb and Mls stimulation of the hybridomas. A small quantitative difference in the sensitivity of hybridoma FJ22.5 to stimulation with V beta 6 or CD3-specific mAb resulted in a marked decrease in efficiency of stimulation by Mls-1a for interleukin 2 production and to inability to detect growth inhibition by Mls-expressing cells. A qualitative difference was observed when analyses of inositol phosphate production were performed under optimal conditions of stimulation of the highly responsive T cell hybridoma (FJ8.1): only stimulation with CD3-specific mAb, but not Mls-expressing cells, could induce detectable inositol phosphate production. Lack of cytolysis of Mls-1a class II-expressing B cells may have evolutionary significance in view of the recent mapping of Mls to mouse mammary tumor virus genes.
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PMID:Evidence for quantitative and qualitative differences in functional activation of Mls-reactive T cell clones and hybridomas by antigen or TcR/CD3 antibodies. 168 Jul 3

The authors performed gene analysis of pulmonary lymphoproliferative disorders. Cell suspensions were obtained from tissues of malignant lymphoma or pseudolymphoma in Cases 1 to 3. High-molecular-weight DNA was extracted from these specimens, digested with restriction endonucleases, size-fractionated by agarose-gel electrophoresis and transferred by the Southern procedure to nitrocellulose. Hybridization to nick-translated 32P DNA probes of the immunoglobulin JH, C kappa, C lambda, regions, and T cell receptor beta 1 region. In case 1 and 2, which were diagnosed as B cell lymphoma, cells from tumor had rearranged heavy chain genes, clearly establishing the clonal nature. In Case 3, which was diagnosed as pseudolymphoma, the tumor contained clonal immunoglobulin gene rearrangements as detected with both the JH heavy chain and C kappa light chain gene probes. It was concluded that gene analysis is an effective procedure for establishing a diagnosis of lymphoma in neoplastic disorders of uncertain cell type and for detecting clonal T cell or B cell populations with atypical lymphofollicular hyperplasia.
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PMID:[Gene analysis of pulmonary lymphoproliferative disorders]. 175 39

Various samples from lymphoproliferative diseases in the skin were analyzed by Southern blotting technique with probes from the T cell receptor gene, immunoglobulin genes, and human T cell leukemia virus-I genome. Samples were taken from 10 mycosis fungoides (MF) patients, 1 parapsoriasis en plaque patient, 10 Adult T cell leukemia/lymphoma (ATL) patients, 1 cutaneous T cell lymphoma (CTCL) patient, 4 lymphomatoid papulosis (LP) patients, 4 B cell lymphoma patients, and 2 actinic reticuloid (AR) patients. In MF, the monoclonality of the T cells became detectable first in the skin when plaques develop to tumors then in lymph nodes, and finally in the blood lymphocytes, indicating this disease develops from local (skin) malignancy to systemic malignancy. In parapsoriasis en plaque, no monoclonality was detected in any sample. We could distinguish cutaneous ATL from the carrier state by detecting the T cell monoclonality and HTLV-I integration with these probes. One patient with CTCL showed detectable T cell monoclonality; 1 out of 4 patients with LP did the same. Four samples from patients with B cell lymphoma revealed detectable monoclonal rearrangement of immunoglobulin heavy and light chain genes. In AR, no monoclonality was detected in any sample. From these data, we conclude that DNA analysis is useful in determining the monoclonality, cell origin, and distribution of monoclonal cells from skin samples.
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PMID:Characterization of the lymphoproliferative diseases in the skin by DNA analysis. 180 May 28

A new non-T cell, non-B cell lymphoma cell line, designated IN-1, was established from the ascitic fluid of a patient with non-Hodgkin lymphoma. The IN -1 cells did not show any T cell and B cell immunophenotypes. There were rearrangements of T cell receptor beta- and gamma-chain gene, but no rearrangement of T cell receptor delta-chain gene and immunoglobulin JH gene. Electron microscopically, the cell had numerous pseudopods, mitochondria, vesicles, a conspicuous nucleolus, and scattered heterochromatin at the periphery of the nucleus. They reacted with only OKT9 monoclonal antibody. Molecular analysis revealed that cellular DNA from the IN-1 cells did not hybridize with Bam HI W fragment of EB virus DNA. Cytogenetic analysis showed that the chromosome number of the IN-1 was in the range of 61 -63 whose karyotype analysis demonstrated multiple numerical and structural chromosome changes. The IN-1 cells were resistant to etoposide in comparison with an IC50 of K562 (human chronic myelogenous leukemia). Interestingly, this IN-1 cell possessed 85 KD protein, but not P-glycoprotein, both of which are considered to be multidrug resistance-related proteins.
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PMID:Establishment and characterization of a non-T, non-B cell lymphoma cell line with T cell receptor beta- and gamma-chain gene rearrangement and possessing MRK 20 monoclonal antibody-defined 85KD protein. 196 85

The value of genotypic analysis for routine assessment of leukaemia and lymphoma was shown by the findings in a selected series of 30 cases. T cell receptor (TcR) gene rearrangements were observed in six out of nine cases of CD3+ CD8+ lymphocytoses and provided clear evidence for clonality in this group. The T cell proliferations in two of the remaining cases masked B cell lymphocytic leukaemia and hairy cell leukaemia, while in the third case no cause was found for the polyclonal proliferation. Heterogeneity of phenotype and genotype were observed in peripheral T cell lymphomas: one out of six cases showed TcR gene rearrangement, one case retained its germline configuration, a further case masked B cell lymphoma and the remainder were polyclonal. Genotypic analysis was helpful in the analysis of a tumour of mixed T cell and myeloid phenotype which was shown to be germline for TcR and immunoglobulin genes, consistent with a myeloid origin. Two histiocytic tumours were found to have clonal rearrangement of TcR genes. Nine out of 11 B cell tumours showed immunoglobulin gene rearrangement. It is concluded that genetic analyses are useful in the analysis of T cell, histiocytic, and B cell tumours in which an immunoglobulin phenotype cannot be defined.
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PMID:Clonality of T cell and phenotypically undefined lymphoid neoplasms: the value of genotypic analyses. 201 33

The staphylococcal exotoxin toxic shock syndrome toxin-1 (TSST-1) has potent stimulatory effects on murine and human lymphocytes. This is the consequence of TSST-1 binding to major histocompatibility complex (MHC) class II molecules and the engagement in a V beta-restricted fashion of the T cell receptor by the TSST-1-MHC class II complex. Using radioligand and functional assays we have recently shown that TSST-1 binds to all HLA-DR (n = 14), HLA-DQ (n = 2) and HLA-DP (n = 2) phenotypes tested. In this study, we have examined the ability of murine MHC class II molecules to bind TSST-1. Specific high-affinity binding of TSST-1 was detectable to unfractionated BALB-c (H-2d) and C57BL/6 (H-2b), but not to C3H (H-2k) spleen cells. The Kd of this binding estimated from Scatchard analysis was in the same nanomolar range as the Kd of binding of TSST-1 to HLA-DR. Binding of 125I-labeled TSST-1 to BALB/c-derived B cell lymphoma lines and to L cell transfectants correlated with the expression of I-A molecules, but not with the expression of I-E molecules. Furthermore, I-A+, I-E- cells but not I-A-, I-E+ cells were able to support TSST-1-induced T cell proliferation. The binding affinity of TSST-1 for I-Ak appears to be much lower than for I-Ad. L cell transfectants expressing hybrid DR alpha: I-E beta k molecules, but not those expressing I-E alpha k: DR1 beta molecules, could bind TSST-1 and efficiently support TSST-1-induced T cell proliferation. This suggests that minor differences in the highly homologous I-E alpha and DR alpha chains are critical in determining the affinity of the MHC class II molecule for TSST-1. These results demonstrate that the binding of TSST-1 to MHC class II molecules in the mouse, in contrast to humans, is strongly influenced by phenotype. Analysis of the molecular basis of these differences may help to localize staphylococcal exotoxin binding sites on MHC class II molecules.
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PMID:Binding of toxic shock syndrome toxin-1 to murine major histocompatibility complex class II molecules. 220 97

A functional analysis of mutant class II molecules was conducted to identify regions important for antigen-specific T cell activation. Site-directed mutagenesis was used to construct a panel of mutant A beta k genes containing either single or multiple d allele substitutions in the beta 1 domain. The product of each of these genes was expressed with either the A alpha d or A alpha k polypeptide in the Ia-negative B cell lymphoma M12.C3. These mutant class II molecule-bearing cells were tested for their ability to present antigen to a panel of Ak-restricted T cell clones specific for various epitopes of myoglobin. Results from this analysis demonstrate that T helper clones recognized complex determinants interacting with multiple residues on the beta 1 domain and also requiring the haplotype-matched alpha 1 domain. This is in contrast to monoclonal antibodies that recognize a domain-specific, immunodominant region involving residues 40, 63, and 65-67. Every T helper clone was found to interact with a distinct pattern of residues, even among clones recognizing the same combination of peptide and major histocompatibility complex (MHC) molecule. The 3 for 1 residue substitution between k and d alleles at residues 65-67 was one of the most important, because it resulted in loss of ability to present antigen to 7 of 7 I-Ak-restricted T cell clones. These residues have been shown previously to comprise the immunodominant allo-specific serological determinants and to stimulate some alloreactive T cell clones. Substitution at residues 12 and 13 also abrogated antigen presentation to all the T cell clones, but this may be a consequence of a conformational change due to altered alpha beta chain pairing. Substitution at position 9, which is predicted to be located in the floor of the peptide-binding groove where it should not interact directly with the T cell receptor, enhanced presentation of the antigenic site 102-118 to some T cells and diminished it to others. This finding suggests a most interesting conclusion that the same antigenic site may bind in different conformations or orientations to the same MHC molecule, although an indirect effect on the conformation of the MHC molecule itself cannot be excluded. Substitutions at residues 85, 86 and 88 also abrogated the response of one T cell clone but not others specific for the same peptide with the same Ia molecule.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antigen presentation to specific T cells by Ia molecules selectively altered by site-directed mutagenesis. 251 56

We determined the configuration of the genes for the beta (T beta) and gamma (T gamma) chains of the T cell receptor in DNA from 100 consecutive cases of B cell lymphoma and B cell chronic lymphocytic leukemia (B-CLL), and compared the findings with those in 18 T cell neoplasms. In 7 of the 100 B cell specimens, a single nongermline band was detected after digestion with the restriction enzyme BamHI, but the rearrangement could be confirmed with a second restriction enzyme in only two. The B cell fragments were small in size and of limited size diversity when compared with the T cell cases, and germline bands of equal intensity were present. A rearrangement of the T gamma gene was never seen in a B cell sample. In contrast, T cell specimens usually rearranged both alleles of T beta (15 of 18), the rearrangement could be confirmed with a second restriction enzyme (17 of 18), both alleles of the first constant region gene segment of T beta always underwent either rearrangement or deletion, and the T gamma gene was also rearranged or deleted (17 of 18). We conclude that ordered rearrangement of the T cell receptor is a rare event in B cell lymphoma and B-CLL. T cell receptor gene studies allow B and T cell lymphomas to be distinguished from each other and from common acute lymphoblastic leukemia antigen-positive non-T, non-B acute lymphoblastic leukemia.
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PMID:Rearrangement of the genes for the beta and gamma chains of the T cell receptor is rarely observed in adult B cell lymphoma and chronic lymphocytic leukemia. 282 Oct 76


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