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

The polyethylene glycol-mediated cell fusion technique has been used to analyze the diversity of the antibody response to the terpolymer poly(Glu60Ala30Tyr10)(GAT). Nine stable clones (all producing IgM K anti-GAT antibodies) were isolated from a fusion between P3-X63-Ag8 myeloma cells and spleen cells from a DBA/2 mouse sensitized to GAT 5 days earlier. Seven other clones (producing IgG K anti-GAT antibodies) were derived from another fusion between NSI myeloma cells and spleen cells of (C57BL/6 X DBA/2)F1 hybrid mice hyperimmunized with GAT. These 16 anti-GAT antibodies were grouped according to their pattern of reactivity with GAT and the two related polymers of poly(Glu60Ala40) (GA) and poly(GLU50Tyr50) (GT). Two monoclonal anti-GAT antibodies (IgM F9-102.2 and IgG F17-148.3) demonstrated crossreactivity with GA but failed to crossreact with GT determinants. In contrast, the remaining 14 hybridoma antibodies demonstrated preferential reactivity with GAT but also exhibited crossreactive binding to GT and in some cases GA. There was a correlation between the fine specificity pattern and the presence of a common anti-GAT idiotype on these antibodies. Thus, the hybridoma anti-GAT antibodies which reacted with GT shared crossreactive idiotypic determinants (CGAT) present in mouse anti-GAT immune sera. In contrast, the monoclonal F9-102.2 and F17-148.3 antibodies that failed to bind to GT lacked the major CGAT idiotypic determinants.
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PMID:Fine specificity of antibodies to poly(Glu60Ala30Tyr10) produced by hybrid cell lines. 8 55

The structures of mouse and human ribosomal DNA were studied using the restriction enzymes Eco R1 and Hind III. Individual mice or humans showed a heterogeneous pattern of restriction fragments resulting from differences in the non-transcribed spacer DNA. Six individual mice from the inbred strain CBA/H-T6 had identical patterns. The same pattern was shown by another CBA strain and by C3H. These strains were originally derived from a BALB X DBA cross made in 1920. Different patterns were found for BALB/c, C57BL and Mus poschiavinus. Cultured cells derived from C3H mice (L cells) showed a pattern quantitatively different from that of the parent strain, but two myeloma cell lines derived from BALB/c showed the same pattern as BALB/c mice. Ribosomal DNA in man is also heterogeneous. Differences were observed between human DNAs in the amounts of the different spacer classes. Studies on mouse-human cell hybrids suggest that some spacer classes are present on more than one of the five human nucleolus organizers.
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PMID:Heterogeneity of the ribosomal genes in mice and men. 56 Sep 12

The serum from non-immunized mice of strains BALB/c, C58, A/He, and RIII contained hemagglutinins for stearoyl inulin-coated SRBC. Immunization with bacterial levan slightly elevated these titers. These same sera also carried cross-specific idiotypic determinants (IdX) that are associated only with inulin-binding myeloma proteins (INBMP) of BLAB/c mice. Three InuldX specificities, A, B, and G, were identified. The InuIdX phenotypes of strains BALB/c, C58, and A/He were InuIdXA+B+G+; strain RIII was InuIdX A+B-G+; strain C57BL/6, C57BL/10, DBA/2, AKR and NH were A-B-G-. Strains CBA, C3H, PL, and C57L could not be typed because of low and inconsistent levels of InuIdX and anti-inulin hemagglutinins. The InuIdXA+B+G+ phenotype was used as a genetic marker in immunoglobulin congenic strains CB-20, BAB-14, and BC-8 and in Bailey RI strains which are derived from crosses of BALB/c (InuIdXA+B+G+) and C57BL/ka or C57BL/6, respectively (InuldXA-B-G-). Linkage of the IdXA+B+G+ to the BALB/c a allotype locus was demonstrated. In addition, the InuldXA+B+G+ marker was used as a phenotype in an analysis of 168 first generation backcorss progeny (C57BL X (C57BL X BALB/c) F). Linkage of the marker to the BALB/c allotype was found again. Two proven recombinant mice having the C57BL a allotype and the InuIdxA+B+G+ markers were identified and progeny tested. Four other potential crossover types are still being progeny-tested.
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PMID:Idiotype of inulin-binding antibodies and myeloma proteins controlled by genes linked to the allotype locus of the mouse. 99 95

A model system is presented for studying the factors involved in tumor immunity. The initial observations with this system concern the importance of dose and route of administration of tumor cells on tumor growth. The data show that myeloma tumor cells, when inoculated i.v.in relatively large numbers, are eradicated by the immune response of an allogeneic host; tumor cells administered i.v. in smaller number escape from immune attack even though the host has the potential to mount an immune response. BALB/c mouse myeloma cells (MOPC-21) were transplanted s.c., i.p., or i.v. into H-2-compatible allogeneic DBA/ 2 mice. There was a marked difference in the response of the host to tumor given s.c. or i.p. as compared to tumor given i.v. Thus s.c. or i.p. inoculation resulted in lethal tumor growth when 5 x 10-3 or more tumor cells were given. In contrast, the outcome of i.v. inoculation depended on tumor cell dose. Although small cell doses ( 5x 10-4 down to 10-2) resulted in lethal tumor gosulted in lethal tumor growth with only 10% survival, large cell doses (10-5 to 5 x 10-7) resulted in tumor rejection and 70% survival. DBA/2 mice possess the immunological ability to react agaist the tumor when large doses of tumor cells (10-7) are given i.v. or i.p., since spleen cells obtained from such mice were found to be able to suppress the growth of MOPC-21 when a mixture of spleen cells and tumor cells was inoculated. On the basis of these initial observations, our model appears to relate especially to the idea that, in autochithonous tumor development or in metastasis of tumor, a small number of antigenic tumor cells, perhaps even a single cell, usually grows into a frank tumor in spite of the immunological competence od the host to respond to the tumor cells.
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PMID:An experimental model for evaluation of factors in tumor escape from immunological attack. 111 32

Two mice DBA/1 were each immunized with a single injection of one million enriched parietal cells in the hind foot pads. Monoclonal antibodies to be used as research tools in studies on regulatory mechanisms in gastric parietal cells were obtained after fusion of mouse myeloma cells (SP2) with cells from the popliteal lymph nodes of the mice. Twelve hybridomas produced antibodies reactive with structures only present in parietal cells as assessed by immunohistochemistry of oxyntic mucosa sections. Three hybridomas were subcloned and the antibodies produced by them, designated as PC4, PC8, and PC117, were characterized. In an enzyme-linked immunosorbent assay, all antibodies reacted with H,K-ATPase-containing vesicles. The antibody PC8 recognized a 94 kDa protein after immunoblotting of H,K-ATPase-containing vesicles and all antibodies precipitated a 94 kDa protein from [125I]H,K-ATPase-containing vesicles. The antibodies PC4 and PC117 recognized extracellular structures with a polarized distribution in viable, purified parietal cells. The results suggest that the structure recognized by all three antibodies is the alpha-subunit of the H,K-ATPase. The antibodies produced by another hybridoma, PC43, recognized a structure present in parietal and surface epithelial cells of the oxyntic mucosa. In an enzyme-linked immunosorbent assay, they reacted with a high-activity carbonic anhydrase which had been affinity-purified from pig oxyntic mucosa and they recognized a 30 kDa protein after immunoblotting. Thus, monoclonal antibodies against both intracellular and extracellular parietal cell structures were obtained after immunization with a small number of parietal cells.
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PMID:Production of monoclonal antibodies against gastric parietal cell antigens. 131 14

Two tumor-associated cellular proteins, 82k/6.3 (MW/pI) and 61k/7.5, which were detected by two-dimensional gel electrophoresis, were studied by biochemical and immunological methods. In two-dimensional gel electrophoresis, 82k/6.3 and 61k/7.5 were rich in colon cancer tissue compared with normal colon mucosa, and they were also detected in fetal intestines. This shows that both proteins might be involved in category of oncofetal proteins. The localization of 82k/6.3 and 61k/7.5 was investigated by subcellular fractionation. They were rich in microsomal fraction, but not found in both nuclear and mitochondrial fractions. In binding reaction with seven kinds of lectins, 82k/6.3 reacted with RCAI, DBA and WGA, where 61k/7.5 reacted with RCAI, DBA, WGA, UEAI and SBA. Transferrin reacted with only RCAI. Each hybrid producing monoclonal antibody against 82k/6.3 or 61k/7.5 was generated by fusing spleen cells of BALB/c mice immunized by the two proteins and mouse myeloma cells. Each monoclonal antibody was specified in enzyme-linked immunoassay. In indirect immuno-fluorescent studies, monoclonal antibodies against 82k/6.3 and 61k/7.5 reacted with cytoplasma and membrane of human cancer cells. This result strongly suggests the localization of the two proteins demonstrated by subcellular fractionation.
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PMID:[Biological and immunological studies on human tumor-associated cellular proteins detected by two-dimensional gel electrophoresis]. 268 83

Acetylcholine (ACh) conjugates were injected into AKR and DBA mice over a period of 10 weeks. The polyclonal antisera were tested at various immunization times for affinity and specificity using an enzyme-linked immunosorbent assay (ELISA). The most immunoreactive compound was found to be choline-glutaryl-bovine serum albumin (or conjugated ACh). The AKR and DBA mice yielding the highest apparent affinity were killed, and the spleen cells were fused with X63 or SP2/O/Ag mouse myeloma cells. Supernatants of confluent cultures were tested for the presence of anti-conjugated ACh antibodies using the same ELISA method. The best results were obtained with the hybridomas from AKR spleen cells and X63 mouse myeloma cells. Monoclonal antibody affinity and specificity were then evaluated by a radioimmunological procedure using iodinated monoclonal anti-conjugated ACh antibody. From competition experiments, the most immunoreactive compound was choline-glutaryl-protein. The other related compounds were recognized either poorly or not at all. The high affinity and specificity of our monoclonal antibody enabled us to visualize ACh molecules on fixed rat brain sections. ACh was fixed with a mixture of nitrobenzyl alcohol and glutaraldehyde. Many ACh-immunoreactive cell bodies and fibers were seen on sections from the basal forebrain and spinal cord. Preadsorption and other immunohistochemical tests demonstrated that the ACh staining was highly specific.
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PMID:Monoclonal anti-conjugated acetylcholine antibody and immunohistochemical applications in rat nervous system. 274 27

Spleens from 1-day-old DBA/2J mice were fused to the nonsecreting myeloma, FO. Dialyzed supernates of these cells were found to suppress the antigen-specific proliferative response of cloned helper or alloreactive T cells at a final concentration of less than or equal to 5%. The same supernate-containing factor did not suppress the response to IL-2 of an IL-2-addicted T cell line. The factor was found not to suppress the production of either IL-2 or antibody, following stimulation of spleen cells with LPS. Absorption analysis revealed that the target of the factor was the accessory cell population. Further experiments indicated that the factor blocked the proliferation of thymocytes due to IL-1. Biochemical analysis revealed a molecular weight for the factor of about 90,000 and a pI of approximately 4.5.
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PMID:NBxFO factor--a novel suppressor factor produced by fusion of neonatal spleen and a nonsecreting myeloma. 297 Mar 5

H-2-linked immune response (Ir) genes control T helper cells (Th) that recognize idiotopes of the V domains of myeloma protein 315 as carriers; Th recognition was detected by augmentation of antibody responses of hapten (4-hydroxy-3-iodo-5-nitrophenylacetyl (NIP]-primed B cells boosted with NIP conjugated to Fab315. The present study indicates that the responder k allele of the Ir VH315 gene maps to the I-A subregion of H-2. A responder s allele of the Ir V lambda 2(315) gene on an A-strain background was identified, which also most likely maps to I-A. Although the d allele of the Ir V lambda 2(315) gene is a responder allele on DBA/2 background, the D2.GD strain (with I-region haplotype AdBbJbEbCb) was non-responder to V lambda 2(315), suggesting either that the responder d allele maps to I-E or that the b allele of a second Ir V lambda 2(315) gene located to the right of I-A exerts a strong suppressive influence. The H-2b haplotype conferred non-responsiveness to VH315, V lambda 2(315), and Fv315.
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PMID:H-2-linked Ir genes have a striking influence on the immunogenicity of idiotopes of myeloma protein 315 for T helper cells. 315 1

Most mammalian cells respond to brief incubation at elevated temperatures by enhanced or new synthesis of a set of heat-shock proteins (hsp). In mouse cells, as determined by SDS--one-dimensional gel electrophoresis, the most prominent hsps have molecular masses of approximately 89,000, 70,000, and 68,000 Da. When the heat-shock response of the mouse erythroleukemia cell line D1B, or two other DBA/2 cell lines (707C1 and 745C2), was examined by [35S]methionine labelling, following heat shocks of 10 min at 42 or 44 degrees C, or 1 h at 45 degrees C, no protein band corresponding to hsp 68 was observed. However, the synthesis of both hsp 89 and hsp 70 was enhanced. Northern blot analysis of cytoplasmic RNA extracted from control and stressed cells indicated that hsp 68 mRNA was absent, even after stresses of up to 1 h at 45 degrees C. Differentiation induced by dimethyl sulphoxide (DMSO) (monitored by the induction of globin synthesis) had no effect on hsp 68 expression in D1B cells; also, hsp 68 could not be induced at various stages of differentiation (0-72 h). Southern blot analysis showed that all three hsp-68 genes were present and not rearranged, and apparently did not carry any deletion in their 5' ends. To determine whether methylation could be involved in maintaining the genes in their silent state, we treated cells with 10 microM 5-azacytidine for 48 h. No hsp 68 expression was observed following such treatment in either undifferentiated or DMSO-induced differentiated D1B cells. Furthermore, Southern blot analysis of MspI/HpaII-digested genomic D1B DNA did not display any differences in methylation patterns around the promoter region of the probed gene compared with control cells, indicating that methylation is not involved in hsp-68 repression. When chimeric plasmids carrying the bacterial chloramphenicol acetyl transferase gene under regulation of the mouse hsp-68 or Drosophila hsp-70 promoters were transfected into D1B cells, minimal (2-fold) or no induction was observed, in contrast with the 60-fold induction seen in a control myeloma cell line. These results suggest a trans-acting mechanism of hsp-68 repression in erythroleukemia cells.
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PMID:The major heat-shock protein hsp 68 is not induced by stress in mouse erythroleukemia cell lines. 317 16


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