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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of serum factors on Ig synthesis (IgE, IgG) in vitro was analyzed. Spleen and mesenteric lymph node cells were obtained from Nippostrongylus brasiliensis-infected and non-infected mice. Sera and ammonium sulphate precipitated serum fractions from mice of different genetic origin (Balb/c - H-2d, A.CA - H-2f, B10.G - H-2q) suppressed in vitro IgE synthesis whereas a pronounced enhancement of IgG antibody synthesis was obtained in several experiments. Our results obtained with sera from both high and low IgE responder strains demonstrated that no strain specificity exists as to the inhibitory efficacy of mouse sera for total IgE synthesis in vitro. The suppressive activity of the mouse sera was concentrated in a fraction precipitated with 20%-50% saturated ammonium sulphate. Amicon XM50 ultrafiltration suggested that this fraction had an apparent molecular weight greater than 50,000 daltons. Suppressive activity was removed by immunoadsorption of the 20-50% fraction with anti-IgE Sepharose. After exogenous addition of monoclonal IgE to an inactive fraction in vitro neither the fraction enriched in IgE nor monoclonal IgE alone were able to suppress IgE synthesis in the culture. Our results suggest that one or more serum factors in the presence of IgE are responsible for the suppression of total IgE synthesis in vitro.
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PMID:Studies on in vitro IgE synthesis from lymph node cells of mice during infection with Nippostrongylus brasiliensis. Presence of inhibitory factor(s) in serum. 380 54

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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PMID: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. 396 44

The kinetics and quality of the alloimmune reaction were studied in CBA (H-2k) mice treated for passive enhancement of tumor allografts (Sa 1 indigenous of A/J (H-2a or H-2k/d) mice). Serum samples of treated animals were tested for their biological properties relevant to different antibody isotypes in vitro (hemagglutination, complement-dependent cytotoxicity, and anaphylaxis, i.e., mast cell degranulation involving all main Ig isotypes; IgM, IgG2, and IgG1, IgE, respectively) as well as in vivo (allograft enhancement). Spleen cells from these treated animals were examined for their capacity to interfere with the rejection of tumor allografts by adoptive transfers into syngeneic recipients. In vitro, 51Cr release cytolysis assays were performed in order to test their cytolytic and regulatory activities in comparison to rejecting control animals. It has been shown that: grafted mice, pretreated for passive enhancement, kept their grafts longer and synthetized anaphylactic antibodies (mainly IgG1) earlier and at higher titers than normal serum controls, which rejected the same Sa 1 allografts. Mice with enhanced tumors synthetized cytotoxic antibodies (mainly IgG2) later than rejecting controls. Serum samples from treated and control animals, harvested 10 days (early sera) and 30 days (late sera) after grafting, were injected with a "normal dose" (0.2 ml) and a "high" dose (0.4 ml) to new CBA recipients grafted with Sa 1. Early immune sera were only enhancing at high doses when derived from animals previously treated for enhancement (at the low dose both immune sera were enhancing). Late sera, presenting both complement-fixing, cytotoxic (predominantly IgG2), and IgG1 anaphylactic alloantibodies in the two groups, induced enhancement in all cases, but more strongly when derived from the group treated for Sa 1 enhancement. Adoptive transfer of spleen cells from animals treated for passive enhancement were able either to inhibit the accelerated rejection (Day 10) or to promote enhancement of Sa 1 allogeneic cells (Day 30) while similar cells taken (Day 10 and Day 30) from control graft-rejecting mice transferred accelerated rejection. Among the transferred T-cell sub-populations, the suppressive effect was mediated by Lyt 2 T cells. In vitro, these spleen cells showed a weaker cytolytic activity than those of allograft-rejecting mice. Moreover, they were able to regulate the cytolytic activity of cytotoxic effector cells from specifically immunized CBA mice.
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PMID:Evolution of alloantibodies and suppressor cells in allografted mice treated for passive enhancement. 402 70

Repeated exposure of rats to an aerosol of ovalbumin (OVA) induced tolerance to subsequent parenteral challenge with the same antigen. In the low-IgE responder WAG strain, responses in both the IgE and IgG classes were affected, whereas rats of the moderate (Lou/M) and high-IgE responder BN strain developed high titers of anti-OVA IgG in serum during exposure with concomitant tolerance in the IgE class. Repeated parenteral challenge, however, failed to elicit significant secondary anti-OVA IgG responses in the Lou/M and BN strains, suggesting that the isotype specificity of induced tolerance in these strains was not absolute. Spleen and respiratory tract lymph node cells, but not serum from aerosol-exposed BN rats, were capable of transferring IgE isotype- and antigen-specific tolerance. Dose response experiments demonstrated that the low-IgE responder WAG strain was exquisitely sensitive to tolerance induction in response to antigen inhalation, being susceptible to dosages in the nanogram range; at least 1000 times more antigen was required in the high-IgE responder BN to induce comparable tolerance in the IgE class. It was also apparent that the IgE isotype was more readily suppressed than the IgG isotype in both high- and low-IgE responder strains.
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PMID:Suppression of IgE responses in inbred rats by repeated respiratory tract exposure to antigen: responder phenotype influences isotype specificity of induced tolerance. 620 36

A method is described for using mini-Marbrook chambers for culturing spleen cells together with anti-idiotype antibody (anti-Id) to induce the appearance of suppressor T cells (Ts). Spleen cells that have been cultured with affinity prepared anti-Id (IgG) but not those cultured with normal IgG, suppress a secondary IgE response to timothy grass pollen antigen B (AgB) when injected intravenously into AGB-primed and boosted syngeneic recipient mice. Suppressor T cells are not induced if the spleen cells cultured with anti-Id are depleted of B cells of if the cells are cultured with the F(ab)2 fragment of anti-Id: both of these results are compatible with Fc+ cells playing a role in the induction of Ts cells by anti-Id. Analysis of soluble suppressor factors in an ELISA test suggests that both TS1 and TS2 cells may be induced by anti-Id.
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PMID:Anti-idiotype regulation of the formation of IgE antibody to timothy grass pollen. II. In vitro induction of suppressor T cells in mini-Marbrook cultures. 621 53

A method using mini-Marbrook chambers in culturing normal spleen cells with timothy-specific T suppressor factor TSF and second order T suppressor factor TSF2 to induce suppressor T (TS) cells is described. Spleen cells cultured with T suppressor factors injected intravenously into recipients primed 20 days earlier with antigen and boosted with antigen within 24 hr of cell transfer, significantly suppress a secondary anti-antigen-B (AgB)-IgE response. On the other hand, spleen cells cultured with normal rabbit IgG failed to suppress the secondary anti-AgB-IgE response in recipient mice. The failure of enriched T cells cultured with either TSF or TSF2 to produce TS cells suggest that an accessory cell may be important in 'presentation' of these soluble factors during the induction of TS cells.
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PMID:Regulation of timothy grass pollen IgE antibody formation. I. In-vitro induction of suppressor T cells by soluble T suppressor factors. 622 66

Spleen cells from Balb C mice immunized with purified Yu human myeloma IgE were fused with NS-1 mouse myeloma cells. After initial EIA screening for antibody-secreting cells, 20 hybrids were further characterized for cell growth, ascites production, antibody titer, specificity and affinity. Immunoglobulins purified from ascites fluid obtained from selected clones were labelled with beta-galactosidase. Combinations were made using either antibodies as capture and as conjugate against calibrated human IgE plasma samples. The combination of monoclonal anti IgE X b 10-22 as a capture antibody and X b 6-16 as a conjugate gave the best sensitivity and slope in EIA. It was successfully used in a sensitive two-step-enzyme-immunoassay for total IgE. The X b 6-16 conjugate was also assayed for the detection of allergen specific IgE antibodies. The results presented and discussed indicate that monoclonal antibodies could favourably substitute for polyclonal anti IgE antibodies in such assays.
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PMID:Monoclonal antibodies to human IgE: utilization for total IgE quantification and estimation of allergen specific IgE antibodies. 639 32

Spleen cells were prepared from Balb/c mice immunized 30 days previously with alum-precipitated ovalbumin (OA), which manifested high, persistent titres of anti-OA IgE and IgG. The adoptive transfer of 5.0 X 10(7) such cells to X-irradiated syngeneic recipients produced comparable persistent IgE/IgG responses, in the absence of secondary antigenic challenge. Fractionation procedures indicated that the nylon-wool adherent population from the spleen was the most active in effecting transfer of the response. However, donor T-cells were also required, as pretreatment of the cellular inoculum with anti-Thy 1.2 antiserum ablated transfer. The inclusion of serum containing anti-OA IgG (but not IgE) in the cellular inoculum also blocked the transfer.
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PMID:Adoptive transfer of "persistent' IgE responses in mice in the absence of secondary antigenic stimulation. 645 6

The protracted IgE anti-ovalbumin (OA) response given by BDF1 mice was studied using an adoptive transfer model. Spleen cells taken from immunized BDF1 mice can produce IgE antibody in irradiated recipients without further overt antigenic challenge. Depletion of macrophages in active spleen cell suspensions did not diminish the capacity of the remaining cells to give an adoptive response. Evidently the cells subserving the adoptive response are not fully developed in donor mice until 4 weeks after immunization, since spleen cells removed at shorter intervals after immunization gave either no or weak adoptive responses. The production of IgE antibody in irradiated recipient mice is prevented if transferred B or T lymphocytes are treated in vitro with either gamma irradiation or mitomycin C, suggesting proliferation of both B and T lymphocytes is essential for the adoptive response to develop. However, the requirement for proliferation is only transient, since one IgE antibody production reached a steady state in the adoptive recipients, it manifested extreme resistance to high dose irradiation. Whole body irradiation of 800 and 1000 rad was without effect on sustained IgE production. This latter observation was valid for both intact mice which were irradiated 8 weeks after immunization and also for irradiated adoptively immunized mice. It is suggested that the IgE anti-OA antibody measured in serum of BDF1 mice several months after immunization with 1 microgram OA and 1 mg Al(OH)3 is the product of long-lived antibody secreting cells.
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PMID:Regulation of the IgE antibody response in mice. II. Radioresistance of established IgE antibody production. 697 4

Conjugates of ovalbumin with Ficoll (OA-Ficoll) were injected into BDF1 mice to establish their immunogenicity and specifically to determine their effect on the IgE anti-OA response. Mice injected with OA-Ficoll responded by producing IgG anti-OA, but not IgE anti-OA. Furthermore, soluble OA-Ficoll injected subsequent to native OA in the form optimal to elicit IgE antibody in fact suppressed the production of IgE anti-OA. Spleen cells from OA-Ficoll-injected mice when injected into normal mice suppressed the subsequent IgE response to OA. OA-Ficoll reacted only weakly with antibody to native OA and had no effect on the IgE antibody response to the unrelated antigen alpha-amylase.
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PMID:Immunogenicity of ovalbumin-Ficoll conjugates with particular reference to IgE antibody production. 739 Jun 33


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