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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Balb/c myeloma proteins, TEPC 15 and MOPC 167, bind phosphorylcholine and precipitate with the C-polysaccharide moiety of pneumococci R36A. Anti-idiotypic antibodies to TEPC 15 myeloma raised in A/He mice prevent plaque formation by cells releasing antibody to phosphorylcholine and inhibit induction of the antibody response to phosphorylcholine in vitro and in vivo. This suppression is specific since antibodies against non-crossreacting idiotypic determinants of MOPC 167 do not prevent either formation of plaques or induction of the antibody response. Furthermore, the response to sheep erythrocytes is not suppressed by antibodies to TEPC 15. These results indicate that antibodies to phosphorylcholine and cell receptors for phosphorylcholine share similar antigen-binding sites with TEPC 15 myeloma protein. Thus, anti-idiotypic antibodies directed against TEPC 15 myeloma protein function as "anti-receptor" antibodies since they specifically prevent induction of the primary response to phosphorylcholine. It is proposed that antibodies to receptors may be involved in the homeostasis of the immune response.
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PMID:Specific suppression of the antibody response by antibodies to receptors. 440 65

The suppressive effects of monospecific goat anti-mouse globulins on primary immunoglobulin class-specific plaque-forming cell responses in mouse spleen cell cultures were investigated. Anti-micro suppressed responses in all immunoglobulin classes, whereas anti-gamma(1) and anti-gamma(2) suppressed the gamma(1) and gamma(2) responses but not gammaM or gammaA responses, and anti-gammaA suppressed only gammaA responses. The mechanism of action of the anti-micro was studied in detail because of its suppression of responses in all immunoglobulin classes. The anti-micro was specific for micro-chain determinants; its activity was dose dependent, but was not mediated by killing cells with surface micro-chain determinants. Free gammaM but not gammaG myeloma proteins in solution effectively competed with micro-bearing cells for the anti-micro. An excess of anti-micro was necessary in the cultures for 48 hr to insure complete suppression of 5-day responses. However, after removal of excess anti-micro at 48 hr, responses could be stimulated by newly added antigen in cultures where incubation was prolonged to 7 days. Anti-micro was most effective when added at the initiation of cultures and had no suppressive effect when added at 48 hr. Excess antigen did not effectively compete with anti-micro for antigen receptors. Precursors of antibody-forming cells were shown to be the cell population where the suppressive activity of anti-micro was mediated. The experiments suggest that anti-micro combines with micro-chain determinants in antigen-specific receptors on the surfaces of antibody-forming cell precursors, prevents effective stimulation by antigen and subsequent antibody production. To explain suppression of responses in all Ig classes by anti-micro, several models were proposed. It is not possible to determine from the data whether stimulation of precursor cells with gammaG or gammaA receptors requires concommitant stimulation of separate cells with only gammaM receptors, or whether cells bearing gammaM receptors are precommitted to or differentiate into cells capable of synthesis of other Ig classes, or whether receptors of gammaM and another Ig class are present on some virgin precursors or the second Ig receptor appears after antigenic stimulation.
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PMID:Immune responses in vitro. IV. Suppression of primary M, G, and A plaque-forming cell responses in mouse spleen cell cultures by class-specific antibody to mouse immunoglobulins. 453 6

Somatic cell hybridization of NS.1 nonsecretor myeloma cells with spleen cells of (DBA/2 X C57BL/6)F1 mice immunized against the myeloma MOPC 70A of BALB/c mice led to the establishment of five hybridoma clones which continuously secrete anti-MOPC 70A cytotoxic antibodies. The respective antigen detected by each of the five monoclonal antibodies is expressed both on plasmacytomas and on antibody-secreting cells as the only normal cell type. The tissue distribution of this new antigen is different from that reported for the alloantigen PC.1, and we have therefore designated it as PC.2. On the basis of immune elimination of direct and indirect plaque-forming cells, all mouse strains tested express PC.2 determinants, identifying PC.2 essentially as an autoantigen. Conventional anti-PC.1 alloantiserum contains antibodies to the PC.2 determinant, and these antibodies are distinguishable from the anti-PC.1 antibodies proper by the fact that only the latter are absorbed by liver cells. Monoclonal anti-PC.2 antibodies are not directed against MuLV-(murine leukemia virus)--associated antigens as over 20 ecotropic, several MCF (mink colony forming recombinant, and xenotropic viruses failed to react in immunofluorescence assays.
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PMID:A new surface antigen (PC.2) expressed exclusively on plasma cells. 615 21

Five monoclonal antibodies were established by the fusion of mouse myeloma cells (NS.1) with spleen cells from A and (A x C3H/An)F1 mice hyperimmunized with 70Z/3 tumor cells. These antibodies recognized a new antigenic specificity provisionally called Ly-m20.2. In direct cytotoxicity assays, 60 percent of cells in spleen, 40 percent in lymph node, 50 percent in bone marrow and less than 5 percent in thymus were found to react with three of the five antibodies, whereas the two others yielded somewhat lower cytotoxicity indices. The Ly-m20.2 antigen was also expressed on cells derived from liver and kidney but not on cells derived from brain. As judged from cytotoxicity assays with separated T and B cells, Ly-m20.2 antigen is carried preferentially on B lymphocytes. Direct plaque-forming cells (PFC) were completely eliminated by Ly-m20.2-specific antibody and complement. Linkage tests by analysis in 20 (CBA/J x C3H/An) x C3H/An backcross mice and by segregation analysis of BXH and SWXL recombinant inbred strains indicate close association of the loci controlling Ly-m20.2 and M1s antigens on chromosome 1.
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PMID:A new mouse cell-surface antigen (Ly-m20) controlled by a gene linked to Mls locus and defined by monoclonal antibodies. 617 19

Monoclonal antibodies directed against antigenic determinants of the New Guinea C strain of dengue-2 virus were obtained from lymphocyte hybridomas produced by fusing immune mouse lymphocytes with mouse myeloma cells. Hybridoma cell culture supernatants were screened by using a radioimmunoassay employing detergent-solubilized dengue-2 infected cell antigens. Monoclonal antibodies in ascitic fluids induced by 22 selected hybridomas were characterized by the hemagglutination-inhibition, plaque reduction neutralization, immunofluorescence, and complement-fixation tests. Both type-specific and broadly cross-reactive antibodies were observed, and immunoglobulin subclasses IgG1 and IgG2a were represented in both groups. At least three distinct antigenic determinants on the virion were defined using these antibodies. A single hybridoma produced antibody which recognized a dengue-2 virus type-specific determinant and exhibited high titered neutralization but had a low titer by hemagglutination inhibition. Four preparations reacted with a type-specific determinant and exhibited hemagglutination inhibition but did not neutralize. Seventeen hybridomas produced antibodies which were broadly cross reactive in all tests. Only two preparations reacted by complement fixation with dengue-2 antigens; both were cross reactive. Immunofluorescence specificity or cross reactivity correlated with neutralization and/or hemagglutination-inhibition. The dengue-2 virus type-specific antibody useful for identification of dengue-2 infected cells by immunofluorescence has been deposited in the Hybridoma Cell Bank of the American Type Culture Collection.
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PMID:Identification of distinct antigenic determinants on dengue-2 virus using monoclonal antibodies. 617 59

Monoclonal antibodies specific for herpes simplex virus type 1 (HSV-1) glycoproteins were used to demonstrate that HSV undergoes mutagen-induced and spontaneous antigenic variation. Hybridomas were produced by polyethylene glycol-mediated fusion of P3-X63-Ag8.653 myeloma cells with spleen cells from BALB/c mice infected with HSV-1 (strain KOS). Hybrid clones were screened for production of HSV-specific neutralizing antibody. The glycoprotein specificities of the antibodies were determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of immunoprecipitates of radiolabeled infected-cell extracts. Seven hybridomas producing antibodies specific for gC, one for gB, and one for gD were characterized. All antibodies neutralized HSV-1 but not HSV-2. Two antibodies, one specific for gB and one specific for gC, were used to select viral variants resistant to neutralization by monoclonal antibody plus complement. Selections were made from untreated and bromodeoxyuridine- and nitrosoguanidine-mutagenized stocks of a plaque-purified isolate of strain KOS. After neutralization with monoclonal antibody plus complement, surviving virus was plaque purified by plating at limiting dilution and tested for resistance to neutralization with the selecting antibody. The frequency of neutralization-resistant antigenic variants selected with monoclonal antibody ranged from 4 X 10(-4) in nonmutagenized stocks to 1 X 10(-2) in mutagenized stocks. Four gC and four gB antigenic variants were isolated. Two variants resistant to neutralization by gC-specific antibodies failed to express gC, accounting for their resistant phenotype. The two other gC antigenic variants and the four gB variants expressed antigenically altered glycoproteins and were designated monoclonal-antibody-resistant, mar, mutants. The two mar C mutants were tested for resistance to neutralization with a panel of seven gC-specific monoclonal antibodies. The resulting patterns of resistance provided evidence for at least two antigenic sites on glycoprotein gC.
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PMID:Antigenic variants of herpes simplex virus selected with glycoprotein-specific monoclonal antibodies. 618 35

Using a plaque assay with immunoglobulin (Ig)-coated SRBC, we and others have previously reported that the majority of polyclonally activated mouse lymphocytes secreted antibodies that appeared to be IgM anti-IgG autoantibodies. Careful reexamination of this assay, with application of several highly purified mouse serum and myeloma IgG and IgM preparations, revealed that IgM, which was a minor contaminant of Ig preparations, rather than IgG, was responsible for the formation of these plaques. High numbers of plaques could also be detected in assays with polyclonally activated human lymphocytes, Ig-coated SRBC, and anti-Ig developing sera. Of all IgG-, IgM- or IgA-secreting cells, 40 to 100% were detected with SRBC coated with gamma-globulin or Ig of the same isotype as the isotype to which the developing serum was specific; in general, low proportions of all PFC were detected with SRBC coated with Ig of a different isotype. Studies on the sequence of events leading to the formation of plaques with Ig-sensitized SRBC (both in humans and mice) revealed that antibodies detected in these assays were not able to bind to the Ig-coated SRBC (without the presence of developing serum), and therefore were not anti-Ig autoantibodies. It is our conclusion that the plaque assays with Ig-coated SRBC represent another type of a reverse hemolytic PFC assay that detects cells secreting antibodies regardless of their specificity, and these plaques are formed due to the cross-linking by the anti-Ig developing serum of the Ig coated on SRBC and the Ig secreted by lymphocytes. Our results confirmed preferential induction of anti-DNA antibody secreting cells in mice by showing that these antibodies indeed bind to DNA coated on SRBC. In cultures of polyclonally activated human lymphocytes, anti-DNA and anti-erythrocyte autoantibody-secreting cells were over 10 to 100 times less frequent than in mice. These results, therefore, disprove the concept of preferential induction of anti-Ig autoantibodies in the polyclonal activation of mouse and human lymphocytes, and show that anti-DNA and anti-erythrocyte autoantibodies are easily induced in the polyclonal activation of mouse, but not human, lymphocytes.
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PMID:Anti-immunoglobulin autoantibodies are not preferentially induced in polyclonal activation of human and mouse lymphocytes, and more anti-DNA and anti-erythrocyte autoantibodies are induced in polyclonal activation of mouse than human lymphocytes. 620 35

The idiotopic repertoire expressed by antigen-specific suppressor T cells (Ts) generated by Streptococcus pneumoniae strain R36a (Pn) in BALB/c strain mice was investigated using a panel of five monoclonal anti-idiotopic antibodies against TEPC-15/HOPC-8 myeloma proteins. Previous studies suggested that the anti-idiotopic antibodies recognize distinct idiotopic determinants within the T15 idiotype, and that Pn-reactive B cells express all of those idiotopes as shown by a specific inhibitory effect of the anti-idiotopic antibodies on induction of anti-Pn response in vitro as well as on the mature antibody plaque-forming cells. In this study we asked the question of whether anti-idiotopic (Id) can block the inductive and/or effector phases of generation of Ts which act on the Pn-reactive B cells. The presence of anti-Id during the activation of T cells with Pn did not prevent the generation of Ts. However, suppression mediated by Ts on responder lymphocytes (cultures of spleen cells or B cels) was inhibited (reversed) by four out of five anti-Id. Some of the antibodies recognize hapten (phosphorylcholine)-inhibitable Id in the paratope of Ig whereas others are directed against nonparatopic Id. These data indicate that the antigen receptor on Ts includes VH sequences both within and without the immunoglobulin in paratope, and that the Id repertoir of Ts overlaps with that of B cells.
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PMID:Immunoglobulin idiotopes expressed by T cells. I. Expression of distinct idiotopes detected by monoclonal antibodies on antigen-specific suppressor T cells. 621 31

The effects of immune complexes on the antibody response of BALB/c mice to Streptococcus pneumoniae R36a (Pn) were investigated. The cell wall polysaccharide (PnC) extracted from Pn was used to form complexes with TEPC-15, a myeloma protein that binds to phosphorylcholine determinants on the PnC. Complexes formed at equivalence were cultured with splenic T cells from BALB/c mice for 2 d, and then the cells were added to fresh BALB/c spleen cell cultures to test their effect on the antibody response to Pn, a response dominated by the T15 idiotype family. The results indicate that TEPC-15/PnC complexes induced potent suppressor T cells (Ts) whereas cells cultured with free antigen or free antibody alone had no effect on the plaque-forming cell response to Pn. The suppression was specific since the response to control antigens such as sheep erythrocytes was unaffected. The suppression appears to be idiotype-specific since the Ts had a relatively weak (and in some cases no) effect on the anti-Pn response of BALB/c mice that had been suppressed for T15 idiotopes by neonatal injection of a monoclonal anti-T15 antibody, MaId 5-4. Furthermore, cells cultured with TEPC-15/PnC complexes were shown to express specific receptors for TEPC-15 idiotopes. The results indicate that antigen/antibody complexes may have important immunoregulatory effects because they are potent inducers of idiotype-specific Ts.
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PMID:Induction of idiotype-specific suppressor T cells with antigen/antibody complexes. 622 33

We report here experiments demonstrating the profound influence of T lymphocytes on isotype expression by B lymphocytes. It was shown that in a secondary in vitro response, T helper cells from primed spleen predominantly induced an IgG1 plaque-forming cell (PFC) response, while T helper cells from primed lymph node induced IgG1, IgG2a and IgG2b PFC responses. Under the same experimental conditions, T helper cell clones were able to induce IgG1, IgG2a and IgG2b responses; therefore, T helper cells are not involved in controlling preferential isotype expression. Stimulated spleen cells were shown to contain T suppressor cells which were able to limit the expression of IgG2a and IgG2b responses. Under certain circumstances, IgG1-specific suppressor cells were also demonstrated. A T-cell hybridoma, T2D4, spontaneously produced the IgG-binding factor, thereby suppressing the expression of the three subclasses studied. Exposure of these cells to IgG1 myeloma protein led to selective enhancement for the production of molecules binding to IgG1, and suppression of the IgG1 PFC response. Similar observations were made with IgG2a and IgG2b myeloma proteins, and the specificity of these isotype suppressive factors was demonstrated. The general significance of these observations is discussed.
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PMID:Control of isotype expression by helper T-cell clones and suppressor cells. 622 38


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