Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spleen cells from CBA or congenitally athymic ("nude") mice were pretreated with various concentrations of DNP coupled to a copolymer of D-glutamic acid and D-lysine (DNP(37)-D-GL), under various conditions of time and temperature. After washing, they were then cultured for 3 days with the direct B cell immunogen, DNP coupled to Salmonella adelaide flagella (DNP-FLA). Under all circumstances tried, exposure of cells to 1 microg/ml DNP-D-GL caused a 70-100% depression in the subsequent DNP-specific PFC response, and 100 ng/ml caused a lesser but still substantial effect. At the concentrations used, DNP-D-GL did not affect irrelevant antibody responses. Though cells from nude mice responded somewhat less well to DNP-FLA than those from CBA mice, no significant difference in the reaction of the two populations to the tolerogen was noted. This demonstrates that DNP-D-GL can, as previously suspected, directly cause unresponsiveness in B lymphocytes.
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PMID:Induction of B cell tolerance in vitro to 2,4-dinitrophenyl coupled to a copolymer of D-glutamic acid and D-lysine (DNP-D-GL). 457 21

Spleen cells of bone marrow chimeras (B cells) and of irradiated mice injected with thymus cells and heterologous erythrocytes (educated T cells) were mixed and cultured together (17). The number of PFC developing in these cultures was dependent both on the concentration of the B cells and of the educated T cells. In excess of T cells the number of developing PFC is linearly dependent on the number of B cells. At high concentrations of T cells more PFC developed; the increase in the number of PFC was greatest between the 3rd and 4th day of culture. Increased numbers of educated T cells also assisted the development of PFC directed against the erythrocytes. It is concluded that the T cells not only play a role during the triggering of the precursor cells but also during the time of proliferation of the B cells; close contact between B and T cells seems to be needed to allow the positive activity of the T cells.
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PMID:Induction of a hemolysin response in vitro. II. Influence of the thymus-derived cells during the development of the antibody-producing cells. 510 56

Spleen cell suspensions of primed donor mice containing precursors of immunocytes have been transplanted into X-irradiated recipient mice 122-138 days after immunization. Following secondary stimulation with antigen (sheep erythrocytes), these precursors, called antigen-sensitive units (ASU), gave rise to progeny cells secreting specific antibody in the spleens of recipients. Single cells releasing IgM hemolysins (direct plaque-forming cells or PFC), IgG hemolysins (indirect PFC), and hemagglutinins (cluster-forming cells or CFC) were enumerated. By transplanting graded and limiting numbers of primed spleen cells, inocula were found which contained one or a few ASU reaching the recipient spleens. We estimated, thereby, the frequency of ASU detectable by our procedures in donor cell suspensions. The values obtained from direct and in-indirect plaque assays, and from cluster assays were 1 in approximately 8.0 x 10(5), 1 in approximately 4.4 x 10(5), and 1 in approximately 5.9 x 10(5) nucleated spleen cells, respectively. The number of splenic ASU for direct PFC was not greater than that of unimmunized mice; however, immunization greatly increased the number of splenic ASU for indirect PFC and for CFC. By applying to each recipient spleen direct and indirect plaque tests and cluster tests, we found that positivity for each type of immunocyte was independent from that of the other two types. These results confirm the unipotent nature of splenic ASU in general, and document the commitment of ASU primed with SRBC to generate progeny cells secreting antibody of a single molecular (IgM or IgG) or functional (lysin or agglutinin) class. We concluded that splenic ASU are composed of relatively differentiated cells of the immune system of mice. With respect to specificity and class differentiation, ASU appear to be as specialized as antibody-producing cells themselves. Our results did not support the view that ASU-derived clonal populations shift from IgM to IgG antibody production.
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PMID:Cellular differentiation of the immune system of mice. II. Frequency of unipotent splenic antigen-sensitive units after immunization with sheep erythrocytes. 578 67

Spleen cells from mice primed to trinitrophenyl-keyhole limpet hemocyanin (TNP-KLH) generate IgG anti-TNP memory responses when stimulated in vitro with either thymus-dependent (TD) or thymus-independent (TI) forms of the hapten. When supernatants from Con A-stimulated spleen cells (Con A Sup) were added to such secondary cultures the TI responses to DNP-dextran or TNP-T4 were augmented; the TD response to TNP-KLH was suppressed. Passage over Sephadex and addition of alpha-methyl-D-mannoside did not inhibit augmentation by Con A Sup, indicating that augmentation did not result from direct action of the lectin on the responding cells. Augmentation occurred equally well in cultures that had been depleted of T cells by treatment with anti-Thy-1.2 and complement. Limiting dilution analyses revealed that Con A Sup increased the frequency of TI-responding precursors approximately threefold while causing a concomitant decrease in TD-responding precursors. To determine the relationship of the additional TI precursors and those normally detected in the absence of Con A Sup, the TI-responding IgG precursors were first eliminated through selective suicide by using DNP-dextran plus BUdR and light treatment; subsequently no TI-responding IgG PFC could be detected to DNP-dextran unless Con A Sup was also added. The data suggest Con A Sup may augment the TI responses to DNP-dextran and TNP-T4 by recruiting additional precursors from a memory cell pool formerly insensitive to these forms of antigen.
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PMID:Concanavalin A supernatant recruits antigen-insensitive IgG memory B lymphocyte precursors into an antigen-sensitive precursor pool. 617 4

The induction and fine specificity of idiotype-specific suppressor T cells (Tsid) were studied. Spleen cells from C57BL/6 mice, immunized 4 wk previously with NP-KLH, failed to express NPb3 idiotype-bearing PFC when challenged in vitro with NP-Ficoll or NP-Brucella abortus. After treatment of NP-primed responder cultures with anti-Thy-1.2 anti-serum + C, NPb idiotype-bearing B cells could be detected. This B cell subset was preferentially suppressed by the addition of T cells from NP-primed mice. With this reconstitution protocol, it was determined that suppression of the NPb idiotype-bearing portion of the B cell response was mediated by a specifically induced T cell population (Tsid) that directly suppressed NPb-bearing B cells. As with a previously described suppressor population induced with hapten-modified syngeneic spleen cells (Ts2), the Tsid population bound and was lysed by NPb idiotype-bearing serum antibodies. However, the Tsid could be distinguished from the Ts2 population because it lacked I-J determinants and functioned as an effector T cell, not an intermediary suppressor cell. Furthermore, fine specificity studies with monoclonal NP-specific antibodies expressing various levels of serologically detectable NPb idiotypic determinants indicated that unlike the Ts2, the Tsid population reacts with conventional, serologically detected members of the NPb family. The combined idiotype binding studies for the Tsid and Ts2 populations demonstrate that the fine specificity of suppressor T cell populations reflects their independent mechanisms of regulation.
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PMID:Characterization of anti-idiotypic suppressor T cells (Tsid) induced after antigen priming. 620 68

Neonatal treatment of A/J mice with DNP-Ficoll reduced or eliminated indirect anti-DNP PFC normally produced in response to adult challenge with DNP-keyhole limpet hemocyanin. The remaining direct anti-DNP PFC response was of low avidity. Spleen cells from neonatal A/J mice inhibited the in vitro but not the in vivo response of adult spleen cells to DNP-Ficoll.
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PMID:Maturation of the lymphoid system. III. Induction of selective unresponsiveness by injection of a haptenated carbohydrate into neonatal mice. 634 Nov 5

Adult female (C57BL/6 X C3H)F1 (B6C3F1) mice were treated with diethylstilbestrol for 14 days and assayed for the ability to produce antibody to a T-dependent antigen, a T-independent antigen, and to respond in vitro to stimulation by a polyclonal activator, bacterial lipopolysaccharide (LPS). No suppression of the in vivo antibody responses were observed. DES produced a subtle alteration in the response to the T-dependent antigen, sheep erythrocyte (sRBC), as treated groups maintained higher PFC values than vehicle groups after the peak day of the response. DES induced an enhanced response to the T-independent antigen, DNP-Ficoll. Spleen cells from DES-exposed animals were only marginally altered in their ability to produce antibody in vitro in response to LPS. Parallel experiments indicated a comparable reduction of LPS-induced blastogenesis. Serum immunoglobulin levels were determined following DES exposure, as a measure of baseline immunocompetence. DES only caused a reduction in the immunoglobulin M (IgM) isotype. DES exposure caused a significant enhancement of the activity of the reticuloendothelial (RES) system. Experiments were performed to assess the effects of enhanced RES function on concentrations of 51Cr labeled sRBC, which were optimal for antibody production. When sRBC were administered i.p., there was no effect on either the Ab response (as reported above) or on the number of sRBC localized in the spleen. In contrast, when sRBC were administered i.v., exposure to DES reduced (approximately 50%) both the Ab response and the number of sRBC localized in the spleen. Enhanced phagocytic function and alterations in antigen distribution must be considered in the interpretation of in vivo immune responses.
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PMID:Effects of subchronic exposure to diethylstilbestrol on humoral immune function in adult female (C3B6)F1 mice. 653 73

Mouse placental extracts (PE) and corresponding Sephadex G-200 fractions were administered to isogeneic CBA mice along with an optimal immunizing dose of SRBC. Spleen cells were harvested 8 days later and transferred to CBA recipients, subsequently immunized with SRBC. The immunoregulatory activity of spleen cells from PE-treated donors was compared to cells from liver extract (LE)-treated controls or from mice immunized with SRBC only, using Cunningham's PFC direct and indirect tests. Within the dose range used, selective modulatory activities were obtained with cells from PE, but not from LE, treated mice, the latter being comparable to cell transfer effects from donors immunized with SRBC only. Spleen cells from animals injected with low doses of PE (0.25 to 4 mg per mouse) added to immunizing SRBC had a suppressive effect on the primary IgM response of recipients immunized against SRBC. In contrast, when SRBC were given to donor animals with higher doses of PE (8 to 13 mg), transferred spleen cells potentiated the IgM response of the recipients. These opposite suppressive and potentiating activities were found in distinct Sephadex G-200 fractions of 40 and 60 kDa, respectively. When the effect of PE treatment was tested within the same animal, the indirect secondary PFC response following a challenge with SRBC was significantly modified. We observed an overall suppression of the different isotypes after treatment with lower doses of PE or with its 40-kDa fraction. PE doses of 0.5 to 2 mg resulted in a stronger inhibition of IgM than IgG1 production. This phenomenon was also obtained with the 40 KDa fraction. IgG2 responses were significantly reduced by all doses of this fraction. In contrast, all doses of the 60-kDa fraction gave a strong stimulation of IgG2 and IgM responses and a constant suppression of the IgG1 response. This shows a clear dissociation between IgG1 and C'-fixing (IgM, IgG2) antibody classes as far as the influence of placental substances is concerned in their regulation. These data emphasize the relevance of isogeneic placental products as a useful physiological material capable of modulating xenogeneic immune responses (as well as allogeneic systems).
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PMID:Modulation of mouse anti-SRBC antibody response by placental extracts. 654 55

Spleen weight, blood counts and anti-SRBC response were estimated in rats subjected to thymectomy and (or) salivary gland extirpation. A significant decrease of spleen weight and number of circulating lymphocytes was observed after thymectomy or salivary glands extirpation. The number of PFC after immunization with SRBC was decreased after thymectomy but not after salivary glands extirpation or, surprisingly, after combined surgery.
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PMID:The influence of salivary glands extirpation and (or) thymectomy on some physiological and immunological parameters in rats. 696 96

Hydroquinone and catechol are two metabolites of benzene that are potential inducers of hematotoxicity. We investigated the in vivo toxicity of these metabolites toward the development of polyclonal, plaque-forming cells (PC-PFC) from progenitor B lymphocytes. Dextran sulfate (DxS), lipopolysaccharide (LPS), or the two mitogens combined (DxS + LPS) were used to induce proliferation and maturation of these progenitors to PC-PFC. Groups of 4 C57BL/6 mice were exposed to 2 daily doses, either intravenously or intraperitoneally, of hydroquinone (100 mg/kg) or catechol (75 mg/kg) for 3 consecutive days. Spleen and marrow cells were harvested for culture 1 day later. The results demonstrated that both metabolites were cytotoxic to spleen cells. Hydroquinone (100 mg/kg) also reduced marrow cellularity, whereas catechol (75 mg/kg) did not significantly affect marrow cellularity. Each compound reduced the frequency of PC-PFC developed from the spleens and marrows of treated mice, but only catechol selectively inhibited the maturation of LPS-activated marrow progenitors into end-stage PC-PFC. These experiments demonstrate the immunotoxic potential of hydroquinone and catechol in vivo through the reduction of progenitor B lymphocytes and suggest that inhibition of precursor cell maturation may play a significant role in the hematotoxicity observed after chronic exposure to benzene.
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PMID:Hydroquinone and catechol reduce the frequency of progenitor B lymphocytes in mouse spleen and bone marrow. 697 15


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