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Z Ovary

Publications and source records attributed to Z Ovary.

At least 37 records · Page 2Linked to original sources
PubMed1987

A novel method to investigate the heterocliticity of antibodies.

Monoclonal and anti-dinitrophenyl and anti-trinitrophenyl IgE antibodies were used to measure heterocliticity using competitive inhibition assays with homologous and heterologous haptens. The antibodies or antibody-containing ascites fluids were diluted to give 50% of the maximum binding to wells of antigen-coated microtiter plates. The % inhibition of binding of the antibody to the antigen by various concentrations of homologous and heterologous haptens at a standard dilution of antibody can then be compared. The advantages of this method of determination of heterocliticity are that it is fast, simple, quantitative and does not need radiolabeled reagents.

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PubMed1987

Regulation of murine IgE production in SJA/9 and nude mice. Potentiation of IgE production by recombinant interleukin 4.

Serum IgE levels were determined in different strains of mice with enzyme-linked immunosorbent assay by using rat monoclonal anti-murine IgE antibodies in normal and in Nippostrongylus brasiliensis-infected mice. After infection, serum IgE levels were high in BALB/c and CB-20, low in SJL/J and SJA/20 mice, and not detected at all in SJA/9 and nude mice. Surface IgE-positive cells were greatly increased in BALB/c and SJL/J mice after infection, but not in SJA/9 and nude mice. Most surface IgE-positive spleen cells were also surface IgM- and surface IgD-positive. When spleen cells from SJA/9 or nude mice were stimulated in vitro with lipopolysaccharide and recombinant interleukin 4 (formerly B cell-stimulating factor 1), IgE was produced and detected in the supernatants of these cultures. In addition, surface IgE-positive cells could be detected in these cultures. Most of the surface IgE-positive cells were surface IgM- and surface IgD-negative, unlike those seen in the spleens of Nippostrongylus-infected BALB/c and SJL/J mice. These observations show that SJA/9 and nude mice have IgE-producing precursor B cells, and after appropriate stimulation interleukin 4 can induce them to secrete IgE.

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PubMed1987

Detection of IgE antibody-forming cells by passive cutaneous anaphylaxis using cell extract from lymphoid organs.

IgE and IgG2a antibody-forming cells in the lymphoid organs of rats were detected by passive cutaneous anaphylaxis (PCA) reaction using the extract from the tissue. The amount of antigen-specific IgE and IgG2a antibodies in the tissue extract could be expressed as PCA titers in which extract from 10(8) cells/ml was used as starting dilution. The total amount of antigen-specific IgE antibody produced in mouse IgE-producing hybridoma cells was calculated by maximum dilution of the extract to the minimal amount of IgE antibody inducing PCA reaction, i.e., 4 ng/ml. In the case of the extract from mouse IgE antibody-forming hybridomas, the minimal number of hybridoma cells to be detected by this method proved to be 2-3 X 10(4) cells/ml.

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PubMed1987

Studies on immunity in hybridoma-bearing mice. A. Immune response to antigens. II. inhibition of production of anti-dinitrophenyl antibodies in mice which have rejected the B 53 anti-dinitrophenyl-producing IgE hybridoma.

When BALB/c mice, which had rejected the anti-dinitrophenyl (DNP) IgE-producing hybridoma B 53, were immunized with DNP proteins, they produced much less anti-DNP antibodies than control (normal) mice. The anti-DNP plaque-forming cell (PFC) number was much less when spleen cells from mice immunized with DNP proteins were treated with sera of mice which had rejected the hybridoma B 53 than the PFC number from the same spleen cells not treated by the sera. The sera of mice which had rejected the hybridoma B 53 contained an inhibitor which was adsorbed and eluted from an anti-mouse immunoglobulin column and also a mouse anti-DNP IgG2a column. The inhibition of PFC was hapten-reversible. In Western blotting the eluates from the anti-DNP IgG2a column reacted as well with the blotted anti-DNP IgE B 53 as an anti-idiotypic antibody to anti-DNP IgE B 53. These criteria establish that the inhibitor in the sera of the mice which had rejected the B 53 tumor was an anti-idiotypic antibody of the type which mimics the epitope (DNP) of the immunizing antigen.

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PubMed1987

The role of mesangial complement in the hematuria of experimental IgA nephropathy.

We sought to determine if codeposits of IgG and IgM and glomerular complement, observed in most cases of human IgA nephropathy, might be important for inducing hematuria. All combinations of three binary variables, the protein immunogen, the duration of oral immunization, and the protein used for intravenous challenge, were accommodated by eight groups of BALB/c mice in an active model of IgA nephropathy. Mice drank 0.1% solutions of either of two proteins for either 6 or 14 weeks, and then were challenged intravenously with either the same protein or the alternate protein. After 6 weeks, all mice had significant increases of serum IgA, IgG, and IgM antibody to the oral immunogen. At 14 weeks, IgG and IgM antibodies were reduced, presumably due to the onset of oral tolerance, but IgA titers persisted. Nearly all mice had mesangial deposits of IgA and oral immunogen. However, only mice immunized for 6 weeks and challenged with the same protein had significant IgG and IgM deposits (100%), C3 deposits (76%), and significant microhematuria. To distinguish between the role of IgG/IgM codeposits and C3 in the pathogenesis of the hematuria, we induced passive IgA nephropathy with immune complexes of monoclonal IgA anti-dinitrophenyl antibody, dinitrophenyl-bovine albumin as antigen, and one of two monoclonal IgG antibodies specific for dinitrophenyl; one of the IgGs fixes complement, the other does not. Despite comparable mesangial deposits of IgA, IgG, and antigen, only mice given immune complexes containing the complement-fixing IgG had glomerular C3 and hematuria. Furthermore, when mice depleted of serum complement via cobra venom factor were given immune complexes containing the complement-fixing IgG, no glomerular complement was observed and no hematuria ensued. We conclude that IgG/IgM codeposits in murine IgA nephropathy do not directly cause hematuria but do induce the deposition of complement, which is in turn required for glomerular injury.

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PubMed1986

Studies on immunity in hybridoma-bearing mice. B. Immunity against the hybridoma. II. The phenotype and specificity of the immune cell.

When appropriate numbers of anti-dinitrophenyl (DNP) immunoglobulin (Ig) E-secreting hybridoma (B 53) cells were injected s.c. into normal BALB/c mice, some of the recipients rejected the tumors. These mice were shown to be immune to B 53 as they withstood, without any ill effect, the i.p. injection of lethal doses of B 53 cells. In previous studies, it was shown that the spleen cells of these mice protected against the growth of B 53 cells. In this study, the characteristics and specificity of the immune spleen cells were examined. The cells responsible for this immunity were shown to be T cells that express Ly-2 on their surface. These cells were shown in in vivo and in vitro assays to limit the growth of the immunizing hybridoma, as well as some but not all BALB/c plasmacytomas and hybridomas.

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PubMed1986

Increased T epsilon cells in BALB/c mice with an IgE-secreting hybridoma.

Since it has been proposed that T cells with receptors for the Fc portion of IgE (T epsilon) in rats, mice and humans are IgE-specific regulatory cells, it was investigated whether mice with an IgE-secreting hybridoma might be a source of large numbers of T epsilon cells. BALB/c mice with ascitic tumors of the IgE hybridoma B53 (epsilon, kappa, anti-DNP) developed high serum concns of monoclonal IgE which was followed by the appearance of large numbers of Lyt1-2+ L3T4- T epsilon cells. In contrast, mice bearing a non-IgE producing variant of B53 failed to develop T epsilon cells. Mice infused with cell-free ascites fluid (containing high levels of monoclonal IgE) from the IgE-secreting B53 hybridoma developed high serum IgE levels and also developed high numbers of T epsilon cells. Mice infused with cell-free ascites obtained from the non-IgE-secreting variant ENP-1 (containing very low amounts of IgE) did not develop either high serum IgE levels or T epsilon cells. These findings suggest that high serum IgE concns induce large numbers of T cells that express phenotypic markers of suppressor cells and have surface IgE-Fc receptors. These studies extend to IgE the principle that hybridomas and plasmacytomas induce large numbers of immunoregulatory T cells that express Fc receptors specific for the heavy chain class of the secreted monoclonal immunoglobulin. Since T epsilon cells are normally present only in small numbers, their marked increase in mice with IgE-secreting hybridomas identifies a ready source of large numbers of T epsilon cells that can be used to investigate their regulatory properties.

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PubMed1985

Suppression of IgE secretion from hybridoma cells in allotype congenic mice: suppression of allotype 7a by T cells in allotype b mice.

Anti-2,4-dinitrophenyl (DNP) IgE producing hybridoma B 53 when injected subcutaneously is established equally well in syngeneic BALB/c (heavy-chain allotype a) and congenic CB20 (heavy-chain allotype b) mice. However, secretion of anti-DNP IgE monoclonal antibody is greatly suppressed in CB20 mice. B 53 cells taken from the subcutaneous tumors of CB20 mice produce anti-DNP IgE in vivo in BALB/c mice and in vitro. No difference was observed in IgE production between these cells and the controls taken from BALB/c mice. The suppression of IgE production was due to T cells and/or their product(s) of CB20 mice.

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PubMed1985

Enhancement of IgE-dependent eosinophil cytotoxicity to dinitrophenylated schistosomula by a nematode infection.

In order to obtain direct evidence for the involvement of IgE in the eosinophil-mediated cytotoxicity, dinitrophenylated (DNP) schistosomula of Schistosoma japonicum coated with monoclonal IgE antibodies were examined as to whether they were killed by rat peritoneal eosinophils. The results indicated that the cytotoxicity of the eosinophils was dependent on a mouse monoclonal anti-DNP IgE antibody, but not on another monoclonal antibody specific to ovalbumin. Moreover, an enhanced cytotoxicity was observed when eosinophils were obtained from rats 4 weeks after infection with Nippostrongylus brasiliensis.

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PubMed1985

Studies on immunity in hybridoma-bearing mice. B. Immunity against the hybridoma. I. Studies on the immune state of mice after rejection of the hybridoma.

Anti-dinitrophenyl IgE secreting hybridoma B 53 cells may be rejected when injected subcutaneously in BALB/c mice. These mice are immune as they withstand without any ill effect the intraperitoneal injection of LD100 B 53 cells. Sera from mice which rejected the tumor have cytotoxic antibodies against the hybridoma, as shown by in vitro tests, but serum cannot transfer immunity to naive BALB/c mice against hybridoma B 53. Spleen cells from mice which have rejected the tumor might transfer immunity against B 53 hybridoma, and with Winn tests it has been shown that these spleen cells are very effective against the B 53 cells and also against the myeloma cells which were used for the fusion to construct the B 53 hybridoma. Subcutaneously injected B 53 cells not only produce anti-DNP IgE secreting tumors, but often also metastasize to spleen, and they are sometimes detected in the circulating blood. Mice with splenic metastasis or with detectable circulating B 53 cells generally die. However, we did observe one mouse with splenic metastasis which successfully rejected the tumor and became immune to B 53 cells.

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PubMed1985

Monoclonal IgE-dependent eosinophil cytotoxicity to haptenated schistosomula of Schistosoma japonicum: enhancement of the cytotoxicity and expression of Fc receptors for IgE by Nippostrongylus brasiliensis infection.

To obtain direct evidence for the involvement of IgE antibodies in eosinophil-mediated killing of schistosomula of S. japonicum, dinitrophenylated (DNP) schistosomula pretreated with mouse monoclonal IgE antibodies were co-cultured with purified rat peritoneal eosinophils. It was found that the eosinophil-mediated adherence and damage to haptenated schistosomula were dependent on a monoclonal anti-DNP IgE antibody, but not on monoclonal anti-ovalbumin IgE antibody. Moreover, eosinophils from N. brasiliensis-infected rats demonstrated an enhanced ability in the IgE-dependent damage to DNP-schistosomula as compared with the cells from normal rats. The enhancement was associated with an increase in the proportion of eosinophils expressing Fc receptors for IgE.

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PubMed1985

Clearance of IgE from serum of normal and hybridoma-bearing mice.

The half-life of IgE in the mouse was investigated by using radiolabeled and unlabeled monoclonal antibodies of the IgE class. Quantitative serologic assays were used for the unlabeled antibodies. IgE was cleared rapidly upon i.v. inoculation; after 48 hr, less than 0.2% of the initial concentration remained in the serum. The IgE was cleared initially with a half-life of 1 to 2 hr, attaining a relatively constant value of 5 to 8 hr. The corresponding values for IgG1, determined as a control, were 11 to 12 hr and 9 to 11 days, respectively. The initial stage probably reflects equilibration with extravascular spaces. This is supported by experiments with mice in which IgE-secreting tumors were implanted and then resected; IgE was cleared from such mice with an average initial half-life of about 5 hr. The rates of clearance of inoculated IgE were approximately the same in mice bearing an IgE-secreting tumor and in normal mice. This suggests that the initial rapid clearance of IgE from normal mice is not due to adherence of IgE to saturable sites; such sites might be expected to be occupied in mice expressing high serum concentrations of IgE. This conclusion was supported by experiments in which 1-mg quantities of IgE were inoculated i.v. into normal mice daily for 6 days. Additional IgE injected on day 7 was cleared normally. The results obtained with tumor-bearing mice indicate that the reported failure to elicit an IgE response to an antigen in mice bearing IgE-secreting hybridomas cannot be attributed to rapid clearance of newly synthesized IgE in such mice, as compared with normal mice.

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PubMed1984

Correlation of murine anti-dinitrophenyl antibody content as determined by ELISA, passive cutaneous anaphylaxis and passive hemolysis.

Antibody contents of IgG1, IgG2a, IgG2b and IgE were measured by enzyme-linked immunosorbent assay (ELISA) in ascites and sera obtained from mice injected with hybridomas producing monoclonal anti-DNP antibodies. In addition, IgG1 and IgE antibodies from sera of immunized mice were also measured by ELISA. Concomitantly, antibody contents were also determined by passive cutaneous anaphylaxis (PCA) in mice for IgG1, IgG2a, IgG2b, by PCA in guinea pigs for IgG2a, by PCA in rats for IgE and by passive hemolysis (PL) for IgG2a and IgG2b. Good correlations were found in the investigated samples between ELISA and the biological determinations.

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PubMed1984

Physiology of IgD. III. Effect of treatment with anti-IgD from birth on the magnitude and isotype distribution of the immune response in the spleen.

Continued treatment with monoclonal anti-IgD (Ig-5a) from birth in BALB/c mice causes a markedly increased responsiveness to i.v. injected dinitrophenylated ovalbumin (DNP-OVA) with Bordetella pertussis at the age of 8 weeks. The 19S plaque-forming cell (PFC)/spleen response is particularly enhanced, 6-8-fold, but all the other isotypes also show increases of 2-6-fold, including IgA and IgE. Both primary and secondary PFC responses and serum antibody titers are enhanced. After transfer of spleen cells from anti-Ig-treated mice to irradiated recipients the IgM/IgG ratio becomes similar to that of controls. In contrast, the response of anti-IgD-treated mice to i.p. immunization with either 0.2 or 100 micrograms DNP-OVA plus alum is reduced by approximately 80% for each Ig isotype except IgM and remains low upon transfer of spleen cells to recipients. It is concluded that the paucity of B cells in peripheral lymph nodes of the anti-IgD-treated mice causes the low responsiveness to i.p. immunization, but that the IgD- B cells in the spleen are quite able to respond and are, in fact, more responsive than IgD+ B cells. This increased responsiveness, together with the higher IgM/IgG ratios for all Ig isotypes and an otherwise similar order of isotype distribution (gamma 1 greater than gamma 2b greater than gamma 2a = epsilon greater than or equal to alpha) as in controls, suggests that a hyperresponsive, but less mature IgD- B cell population is selectively produced in the spleens of mice treated with anti-IgD from birth.

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PubMed1984

Studies on immunity in hybridoma-bearing mice. A. Immune response to antigens. I. Role of subcutaneously injected IgE-producing hybridoma on antibody production of different isotypes against immunizing antigens.

When immunized with ovalbumin (OVA), mice bearing subcutaneously injected anti-dinitrophenyl (DNP) IgE-secreting hybridoma cells do not produce anti-OVA IgE antibodies as long as anti-DNP IgE is present in abundance in their sera. As soon as the titer of anti-DNP IgE antibody falls, anti-OVA IgE antibody appears. This inhibition of production of anti-OVA IgE is attributed to Fc epsilon-bearing T cells which have a suppressive action of limited duration. Other isotypes of anti-OVA antibodies are produced in similar amounts as in controls which were immunized with OVA but not injected with hybridoma cells.

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PubMed1984

Isotype IgE class-specific suppression in the Biozzi 'High' and 'Low' lines of mice.

The suppression of the production of IgE antibody was investigated with the Biozzi 'High' and 'Low' lines of mice. Using the adoptive transfer method formerly experimented with SJL mice (donor I immunized with 0.2 microgram dinitrophenylated ovalbumin, donor II hyperimmunized with 10 micrograms keyhole limpet hemocyanin and donor III being unimmunized mice) IgE suppression was observed in recipients irradiated with 600 R only with the 'Low' line.

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