Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A sequential change in the number of circulating immunoglobulin (Ig) secreting cells of each Ig class following blood transfusion was studied using a reverse hemolytic plaque assay. The subjects studied were in two main groups, immunologically normal individuals and patients with malignant lymphoma or multiple myeloma who are, presumably, immune incompetent. A consistent increase in circulating IgG-secreting cells, along with either an earlier or simultaneous increase in IgM-secreting cells, was observed following blood transfusion in the immunologically normal individuals. An increase in IgA-secreting cells was also observed, but at a minimal magnitude. Such an increase was not apparent in patients with lymphoma or myeloma. The possible use of blood transfusion as a means of "challenging and checking" for the state of immune responsiveness in vivo is discussed.
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PMID:Increase in the number of lymphocytes secreting IgG following blood transfusion. 703 13

Anti-idiotypic antibodies (a-Id) were produced in syngeneic mice against two monoclonal IgM antibodies of BALB/c origin, TNP. 11 and SP/603. In plaque inhibition tests, using IgM-secreting hybridoma cells and anti-idiotypic antibodies, these two IgM proteins, as well as the anti-TNP myeloma protein MOPC 460 (IgA) were found to carry non-cross-reactive idiotypes. Analysis of the anti-trinitrophenyl (TNP) plaque-forming cells (PFC) in BALB/c mice, either normal or immunized with TNP-horse red blood cells, revealed that in addition to the MOPC 460 Id, also the SP/603 Id is recurrent and expressed by a fraction of the anti-TNP antibody-secreting cells in all individuals tested. In contrast, the TNP. 11 Id could not be detected in any BALB/c mouse studied. TNP. 11 and SP/603 antibodies were then characterized by their ability to induce an antigen-independent anti-TNP response in normal BALB/c mice. While TNP. 11 was found to be inactive, the same titers of SP/603 IgM induced antigen-specific PFC all of which expressed the SP/603 Id, and increased titers of circulating IgM molecules carrying the same Id, suggesting that "recurrent" but not "nonrecurrent" Id are competent in this respect. A fraction of these SP/603-induced, SP/603-positive anti-TNP antibodies also carried MOPC 460 Id, suggesting expression on the same molecule of idiotypic determinants found on independent non-cross-reactive "recurrent" idiotypes.
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PMID:Antigen-independent, IgM-induced antibody responses: requirement for "recurrent" idiotypes. 704 74

The pokeweed-mitogen-induced transformation of B-lymphocytes into immunoglobulin-secreting cells was studied in vitro in 25 patients with multiple myeloma using a reverse hemolytic plaque assay. Fifteen patients showed a good response in generating immunoglobulin-secreting cells, whereas 10 patients showed a decreased B cell reactivity which was not due to intermittent melphalan/steroid therapy administered to 15 patients. Experiments with lymphocyte subpopulations demonstrated that the inability of some multiple-myeloma patients to generate immunoglobulin-secreting cells was always based on a defect in the B-cell subset. Co-culture experiments with lymphocytes from normal individuals and patients revealed a cell-mediated suppression in one case, whereas humoral suppressive factors in the patients' serum could not be observed using the reverse hemolytic plaque assay. Patients were classified into three groups: (a) patients with a normal B-cell function, (b) patients with a reversible, tumor-dependent suppression of B-cell reactivity and (c) patients in whom the normal B-cell population was replaced by non-reactive cells.
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PMID:PWM-induced generation of immunoglobulin-secreting cells in patients with multiple myeloma. 704 86

Different clones of mouse hybridomas, derived from the fusion of unstimulated mouse peritoneal cells with mouse myeloma cells, producing IgM monoclonal antibodies directed against the membrane of bromelain-treated mouse erythrocytes (MRBC(Br)) have been previously established. We have recently shown that one of these hybridomas produce, in ascites, antibodies cross-reacting with phosphorylcholine derivatives (trimethylammonium (TMA) derivatives). In this work the cross-reactivity for TMA derivatives of the monoclonal antibodies produced by 4 anti-MRBC(Br) hybridomas have been studied at the cell level (plaque-forming cells). Phosphorylcholine, choline bromide and p-aminophenyl-trimethylammonium were found to be potent specific inhibitors of plaque formation (anti MRBC(Br)). The hemolytic activities of ascites and tissue culture supernatants were studied and their inhibition by TMA derivatives was determined. Immunoglobulins from ascites purified on TMA immunoadsorbent column were analyzed by two-dimensional gel electrophoresis, their spectrotype was compared to the spectrotype of immunoglobulins from tissue culture supernatants from the same hybridoma radioactively tagged by internal incorporation of [14C]leucine. It could be shown without ambiguity that the PTMA column retained an IgM with the same characteristics as the IgM secreted in vitro.
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PMID:Relationship between choline derivatives and mouse erythrocyte membrane antigens revealed by mouse monoclonal antibodies. I. Anticholine activity of anti-mouse erythrocyte monoclonal antibodies. 715 55

Idiotype analyses of plaque-forming cells using anti-idiotype antibody against TEPC-15 myeloma protein (anti-T 15 id) indicated that the proportion of plaque-forming cells producing anti-phosphorylcholine (PC) antibodies with idiotypic determinants of T15 id varied depending on the strain of mice (15-97%). However, treatment of neonates of those mouse strains with the anti-T 15 id antibody rendered them unresponsive to subsequent stimulation with PC-containing antigen (less than 7% of control response). The treatment of spleen cell cultures, derived from adult mice, with anti-T 15 id antibody resulted in complete suppression of T 15 id, although the suppression of the total anti-PC response was much less pronounced as compared to that induced in vivo. These results suggest that anti-T 15 id antibodies injected in the neonatal period may chronically inhibit the differentiation of B lymphocytes specific for PC. The lack of compensatory increases in the production of anti-PC antibodies bearing other idiotypes in T 15 id-suppressed mice does not appear to be related to the clonal proportion of cells producing anti-PC with non-T 15 id. This tolerance induction by anti-idiotype antibody appears to be unique to the nature of clonal differentiation of anti-PC-producing lymphocytes.
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PMID:The lack of compensatory increases of cells producing anti-phosphorylcholine antibodies bearing other idiotypes in TEPC-15 idiotype-suppressed inbred and outbred mice. 718 13

A slid-phase radioimmunoassay (RIA) for assaying immunoglobulin produced from antibody-secreting myeloma, hybridoma and immune spleen cells is described. Specific antibody is detected by culturing antibody-producing cells on antigen-coated flexible polyvinylchloride microtiter wells, washing away the cells, and measuring the bound specific antibody with tritiated affinity-purified anti-isotype reagents. Antibody produced from 10(3) myeloma cells can be detected with as little as 4 h of incubation. With 24-48 h of incubation, antibody from as few as approximately 3-15 myeloma, hybridoma or immune spleen plaque-forming cells (PFC) can be detected. This culture-well RIA has certain distinct advantages over the hemolytic PFC assay and RIA assays in which antibody in culture supernatants is measured.
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PMID:Use of a solid-phase 3H-radioimmunoassay for the measurement of immunoglobulin produced in short-term cultures of antibody-secreting cells. 719 47

The role of secretory antibody in protection against respiratory syncytial virus (RSV) infection was examined by using monoclonal immunoglobulin A (IgA) antibody for intranasal passive immunization of mice. Eight anti-RSV IgA hybridomas were produced by fusing myeloma cells with lung lymphocytes from RSV-immunized mice. Five IgA antibodies recognized RSV strains of both the A and the B subgroups, and two of these neutralized virus in a plaque reduction assay. Monoclonal IgA antibody HNK20, which bound to F glycoprotein, was most effective, reducing plaques by 50% at a concentration of 0.1 microgram/ml for both subgroup A and subgroup B strains. HNK20 also neutralized all of eight clinical isolates of RSV tested. When delivered intranasally to mice 24 h prior to RSV challenge, HNK20 reduced virus titers in the lungs by nearly 100-fold. Maximal protection occurred at a dose of 0.5 mg/kg of body weight. Significant protection against lung infection was seen when the interval between antibody treatment and challenge was as long as 72 h. HNK20 also decreased virus titers in the nose approximately 10-fold when given 1 h, but not 24 h, before challenge. When mice were treated with HNK20 intranasally 3 days after challenge, viral titers were reduced in the lungs but not the nose. The results indicate that topical application of relatively small amounts of monoclonal IgA can protect against both upper and lower respiratory tract infections caused by RSV.
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PMID:Intranasal monoclonal immunoglobulin A against respiratory syncytial virus protects against upper and lower respiratory tract infections in mice. 769 63

Novel compounds based upon the thiol N-(carboxy)-beta-alanyl-cysteamine (vitaletheine) have strikingly potent and seemingly diverse biological activities. Concentrations of vitaletheine modulators from 1 femtograms/ml to 100 picograms/ml medium regulate RBC production from progenitors initially deprived of erythropoietin. Similarly, as little as attograms/ml concentrations of the disulfide vitalethine stimulate immunological responses of murine splenocytes toward sheep RBC in a hemolytic plaque assay. Because dosages of vitalethine as low as femtograms/kg substantially diminish tumor size and incidence and increase survival to 80% in mice inoculated with a uniformly fatal melanoma (Cloudman S-91), activities of these compounds have in vivo significance. A preliminary probe of the benzyl derivative of vitalethine in a myeloma model (NS-1) suggests efficacy (100% survival) as well. The high potencies of the vitaletheine modulators, both in cell culture and in vivo, indicate that these or similar regulatory components, if constitutively present, probably occur endogenously at vanishingly small concentrations and may be prone to deficiency resulting from metabolic imbalances, irradiation, aging, diet, pathogenic or parasitic infections, or exposure to environmental pollutants. Pathways for the biosynthesis of vitaletheine are proposed and chemical syntheses of the vitaletheine modulators are described. Possible molecular mechanisms of action, including interactions with peptidyl hormones, other endogenous effectors, and xenobiotic and pharmaceutical compounds, are explored. Indications for the treatment of other diseases are identified.
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PMID:Vitalethine modulates erythropoiesis and neoplasia. 792 8

beta-Alethine (beta-alanyl-cysteamine disulfide) exhibits striking biological activities in diverse systems. At an optimum of about 10 ng/ml, beta-alethine (a) adapts murine liver cells to culture (53 colonies/10(6) cells versus none in controls), (b) delays aging of human IMR-90 fetal lung fibroblasts (102 population doubling levels versus 47 in controls, producing 3 x 10(16) greater biomass), and (c) markedly stimulates antibody-producing plaque-forming cells from murine splenocytes (16,875/10(6) cells versus 55/10(6) cells in controls) or human peripheral blood leukocytes (1826/10(6) cells versus 0/10(6) cells in controls). Early interventions with beta-alethine (1 ng/kg to 100 micrograms/kg) successfully treat NS-1 myeloma in a syngeneic murine tumor model (NS-1 myeloma). Although there are indications in this model that beta-alethine is also effective when intervention is late, beta-alethine is ineffective in an allogeneic murine melanoma model (Cloudman S-91 melanoma). It is inferred that beta-alethine enhances cellular phenotypic expression, function, and vitality in diverse biological systems and may treat certain types of neoplasia. Because atomic spacings between the amide moieties in beta-alethine are the same as in the differentiating agent hexamethylene-bis-acetamide and because the radioprotectors WR 2721 and WR 1065 lack only the carbonyl oxygen of the thiol form (beta-aletheine), biological activities already reported for these compounds are compared with those presented herein for beta-alethine. Although these comparisons have not been made in the same systems, the tentative conclusion is that the amide moieties of beta-alethine may be critical to its potency and lack of obvious toxicity in cell culture and animal models.
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PMID:Seemingly diverse activities of beta-alethine. 792 9

A simple, convenient method employing a gE-specific neutralizing monoclonal antibody (mAb; FTpn3) for isolation of the gE gene-deleted recombinant pseudorabies virus (PRV) is described. FTpn3 secreting hybridoma was obtained by fusing PRV-immunized BALB/c splenocytes with myeloma cells. To construct gE gene deleted PRV, a 5.7 kbp DNA fragment with deletion of the gE gene was engineered and cloned. The plasmid was then used for cotransfecting Vero cells with wild-type PRV genome. The resulting viruses were subjected to FTpn3 neutralization. The FTpn3 resistant virus was isolated and plaque purified further. By DNA fingerprinting and Western blotting analysis, the virus resistant to FTpn3 neutralization was proved to be the gE-deleted recombinant virus.
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PMID:Isolation of gE gene deleted pseudorabies virus by using a gE specific monoclonal antibody. 879 2


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