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 and other lymphoid tissues of rabbits immunized with human serum albumin (HSA) and human lactoferrin (LF) were examined for the presence of cells forming anti-idiotype antibodies. To detect these cells, IgG, F(ab')2, or Fab' of specific antibodies were isolated, fluorochrome-tagged with tetramethylrhodamine isothiocyanate, and used as an idiotypic marker to detect splenic plasma cells that are producing anti-idiotypic antibody. By this procedure, we were able to demonstrate anti-idiotypic cells in surprisingly high numbers. For example, in six rabbits immunized with HSA for periods ranging from 36 to 542 d, the percentage of Ig-positive cells that stained with autologous idiotype ranged from 0.7 to 44; furthermore, cross-reactivity was observed among seven different anti-HSA preparations and two anti-LF antisera. The isotype of anti-idiotypic cells, determined by costaining with fluorescein isothiocyanate-labeled goat Fc-specific anti-rabbit Ig, was shown to be predominantly IgG. These findings provide evidence of the presence of plasma cells producing antibody to autologous idiotype during a vigorous immune response.
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PMID:Presence of plasma cells binding autologous antibody during an immune response. 9 59

Spleen T-cells of mice immunized intravenously with gamma-irradiated allogenic lymphoid cells at a high dose are shown to inhibit the activation of DNA synthesis in MLC. The difference in the whole H-2 complex or in either of its K, I, D regions or I-subregions is required and sufficient for induction of specific T-suppressors. The magnitude of the suppression is a sum of suppressive reactions induced separately by each of the immunizing complex components, the products of one of the H-2 regions (subregions) as shown by changing the source of stimulator cells in MLC. These components have a similar impact in the suppressor activity. Unlike the other T-cell subclasses, T-suppressors react only to serologically defined mutant antigens of the Dd allele, but do not react to the mutants of the Kb allele and do not discriminate Kb and Kba antigens. Specific suppressor T-cells recognize the I-subregion products without their linkage to the K/D region products. For elicitation of the suppression two conditions are required and sufficient: a) direct contact of immune suppressors with the corresponding antigenic determinant; b) the subregion IC identity between the suppressors and the responder cells. Intensity of suppression is reduced if F1 hybrid responder cells interact with parent suppressor cells, but is not reduced in the inverse arrangement of the experiment. Specific suppressor T-cells are presumed to differ from other subclasses of T-cells and to be similar to B-cells relatively to the nature and multiplicity of recognizable individual products of the H-complex and to narrow specialization of reactive clones.
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PMID:[Genetic conditions for the induction and realization of the action of specific T-suppressors immune to H-2 antigens]. 9 36

The localization of a major determinant on an isologous myeloma protein (M315) which stimulates BALB/c helper T cells was investigated. Augmentation of the adoptive secondary antibody response to NIP-M315 and the idiotype of M315 (Id315) was used as an indicator of helper effects. Spleen cells primed with the light chain of M315 (L315) and its V-domain (VL315) were highly efficient helpers; priming with the fragment containing the two V-domains of M315 (FV315) induced a somewhat weaker helper effect than L315 or VL315. The helper effect was abolished or markedly reduced by treating the primed cells with rabbit anti-brain theta + C. Cells primed with the heavy chain of M315 (H315) effected weak but significant help. The V-domain of H315 (VH315) was incapable of eliciting cells with detectable helper effect. The data indicate that the VL315 embodies a major determinant for T helper lymphocytes. This determinant is expressed on the free VL315 as well as on the complete M315. In contrast, previous studies have shown that BALB/c antibodies produced against Id315 recognize antigenic sites that are only displayed on associated (VL315 + VH315) domains.
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PMID:T helper lymphocytes recognize the VL domain of the isologous mouse myeloma protein 315. 9 75

CBA and C57BL mice both possess a VHdex gene coding for antibodies against the alpha 1-6 epitope of dextran B512. After immunization with dextran, CBA mice produce IgM plaque-forming cells (PFC) only, which show regular cyclical fluctuations. The second PFC peak disappeared after injection of dextranase, indicating that it is antigen-dependent. The anti-dextran response in C57BL mice is characterized by only one IgM peak, followed 1 day later by an IgG peak that may exceed the IgM response by a factor of 10. The IgG anti-dextran response in C57BL mice was thymus-independent. CBA mice gave an IgG response to the hapten fluorescein isothiocyanate (FITC) after immunization with FITC-dextran, indicating that dextran can function as a carrier for an IgG response in this strain. Attempts to induce IgG PFC against dextran by immunizing CBA mice with thymus-dependent dextran-protein conjugates consistently failed, althouth the conjugates induced IgG fc in C57BL mice. Spleen cells from CBA mice failed to produce IgG antibodies against dextran after transfer into lethally irradiated C57BL mice, whereas the C57BL spleen cells produced IgG PFC after transfer into CBA mice. The lack of IgG synthesis against the alpha 1-6 epitope of dextran in CBA mice appears to be regulated exclusively at the B cell level and is restricted specifically to the VHdex gene product.
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PMID:A thymus-independent IgG response against dextran B512 can be induced in C57BL but not in CBA mice, even though both strains possess a VHdex gene. 9 95

Murine and human beta 2-microglobulin (beta 2m) bind to various types of mouse cells. The binding is saturable and displays a single association constant of about 1 x 10(9) liter/mol. The binding of beta 2m to splenocytes was not affected by a variety of metabolic inhibitors but was temperature-dependent. It is suggested that the beta 2m "receptor" exhibits a temperature-dependent conformational change since the "receptor", whether integrated into the membrane or solubilized by the detergent Triton X-100, binds beta 2m poorly at low temperatures. Spleen T and B lymphocytes display more binding sites than thymocytes, kidney, liver and brain cells. The relative amounts of the beta 2m-binding "receptor" on these cell types are strongly correlated to the relative amounts of H-2 antigens. This correlation is also obvious for the teratocarcinoma cell line F9, which lacks both beta 2m "receptor" and H-2 antigens, but spermatozoa, which express very small amounts of H-2 antigens, have an appreciable amount of the beta 2m "receptor". The latter observation, together with the fact that alloantisera directed against H-2 K and D antigens do not measurably affect the binding of beta 2m to the "receptor", may argue against the notion that the beta 2m "receptor" represents H-2 antigens which have lost their endogenous beta 2m. Normal mouse serum contains a component which inhibits the binding of beta 2m to splenocytes. It is likely that this serum protein is identical to a newly discovered H-2 antigen-like glycoprotein. The beta 2m "receptor" appears to be under the control of the major histocompatibility complex as splenocytes of the H-2f haplotype bind considerably more beta 2m than splenocytes of other haplotypes.
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PMID:Demonstration of a murine cell surface component with affinity for exogenous beta 2-microglobulin. 9 8

This communication describes a method to obtain enriched populations of T-cells, B-cells and macrophages. Spleen cells were initially fractionated on nylon wool columns. The nylon wool adherent fraction was removed by mechanical agitation and further separated on the basis of adherence to a coated-plastic surface in the presence of autologous serum. The tissue flask adherent population was removed with the aid of a rubber policeman. The nylon wool non-adherent and the tissue flask non-adherent and adherent fractions were characterized for the presence of cell surface markers, size, and functional activity and were identified as T-cells, B-cells and macrophages, respectively. The two-stage adherence procedure is simple to perform and does not require sophisticated equipment or expensive reagents.
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PMID:Isolation of T-cells, B-cells and macrophages by a two-stage adherence procedure. 9 9

Mouse thymuses with more than 99% T cells have been reported to contain immunoglobulin kappa mRNA-like molecules (kappa RNA) in relatively large quantities. The present study was undertaken to rule out the possibility that the kappa RNA was mainly a product of a few contaminating B cells of the thymus and to determine whether all T-cell subpopulations contained kappa RNA. By in situ hybridization with DNA complementary to kappa mRNA (kappa cDNA) the following observations were made: 98.5% of thymus cell preparations hybridized with kappa cDNA; the 1.5% unlabeled cells were generally larger and paler staining than the majority of thymus cells. Only 0.015% of thymus cells were intensely labeled and appeared to be plasma cells. Also, 87% of spleen cells hybridized with kappa cDNA; most of these showed similar labeling intensity to the majority of thymus cells. The number of unlabeled cells corresponded to the percentage of hemopoietic cells and macrophages in the spleen. Spleen cells in the range of 0.37-0.85% were intensely labeled and appeared to be plasma cells. The following controls supported the conclusion that the results with thymus and spleen were due to specific hybridization: most of the kappa mRNA-deficient tissue culture cells of the plasmocytoid tumor ABPL-4 did not hybridize with kappa cDNA. The kappa mRNA-producing cells from myeloma PC 3741 hybridized in situ with kappa cDNA. Furthermore, all cells from this tumor and all spleen cells hybridized uniformly with a cDNA probe complementary to most of the total cellular poly(A)-containing RNA species of these cells. These results indicate that T cells of all types in the thymus as well as in the periphery contain substantial quantities of kappa RNA.
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PMID:Direct demonstration of immunoglobulin kappa chain RNA in thymus T cells by in situ hybridization. 9 43

The aim of this study was the identification of the cell type in which genes selected for high or low response to SRBC express their functions. Spleen cells from high (H) and low (L) responder mice were immunized with SRBC in the Mishell and Dutton system. An antibody response of different magnitude was found in cultures of H and L spleen cells, the difference being at least as great as that observed in vivo. This finding under experimental conditions allowing the exclusion of any influence of the animal milieu during the immune response, suggest macrophages, B, and T lymphocytes as possible target cells of gene action. In vitro cell separation and recombination experiments in which spleen cells were immunized with SRBC, TNP-LPS, or TNP-HRBC indicate that the genetic differences between H and L responders brought about by selective breeding are expressed in lymphocytes to greater extent than in macrophages. The role of histoincompatibility in the recombination experiments in unlikely but cannot be excluded. Among lymphocytes, B cells but not helper T cells were found more responsive in cultures of spleen cells from H than from L mice.
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PMID:In vitro immune response of spleen cells from mice genetically selected for high or low antibody production. 9 27

The possibility was investigated that Ir genes regulate the function of cells other than T or B cells in the primary IgM responses to the synthetic antigens trinitrophenylated poly-L-(Tyr,Glu)-poly-D,L-Ala--poly-L-Lys [TNP-(T,G)-A--L]and trinitrophenylated poly-,-(His,Glu)-poly-D, L-Ala--poly-L-Lys [TNP-(H,G)-A--L]. The primary responses of (B10 x B10.A)F(1) spleen cells to both antigens were abrogated by Sephadex G-10 passage, and restored by the addition of spleen adherent cells. The cell type in the spleen adherent cell population active in reconstituting the responses to TNP-(T,G)-A--L and TNP-(H,G)-A--L was a non-T, non-B, radiation-resistant, glass-adherent spleen cell. The responses of Sephadex G-10-passed (responder x nonresponder)F(1) spleen cells to TNP-(T,G)-A--L or TNP-(H,G)-A--L were reconstituted by spleen adherent cells from only responder strains. Spleen adherent cells from F(1) mice reconstituted the responses to both antigens. Spleen adherent cells from each of the strains tested reconstituted the non- Ir gene-controlled response to a third antigen, TNP-keyhole limpet hemocyanin. The inability of spleen adherent cells from nonresponder strains to reconstitute the responses to either TNP-(T,G)-A--L or TNP-(H,G)-A--L was not a result of active suppression induced by the presence of nonresponder adherent cells, since a mixture of responder and nonresponder spleen adherent cells reconstituted the responses to both antigens. The use of spleen adherent cells from recombinant strains demonstrated that the autosomal dominant genes controlling the ability of spleen adherent cells to function as accessory cells in the responses to TNP-(T,G)-A--L and TNP-(H,G)-A--L are located in the K or I-A regions of the responder H-2 complex, the same region(s) of H-2 as the Ir genes controlling overall in vitro and in vivo responsiveness to these antigens.
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PMID:Cellular and genetic control of antibody responses in vitro. III. Immune response gene regulation of accessory cell function. 9 11

The response of spleen and peripheral blood lymphocytes (PBL) to mitogen stimulation with phytohemagglutinin (PHA), Concanavalin A (ConA), and pokeweed mitogen (PWM) was determined for owl monkeys (Aotus trivirgatus) experimentally infected with the Vietnam-Oak Knoll (FVO) and the Uganda-Palo Alto (FUP) strains of Plasmodium falciparum. PBL from Panamanian Aotus monkeys with less than 25% FVO infection responded normally to mitogen stimulation; however, increased parasitemia of 25--50% resulted in a significant suppression of ConA responsiveness. Colombian Aotus monkeys infected with the PUF strain also developed a suppression to ConA stimulation but with a lower parasitemia (10--25%). When the parasitemia became greater than 50% in these animals, PHA, ConA, and PWM responses were significantly decreased in cultures of PBL. Spleen cells from all acutely infected Aotus monkeys were suppressed to PHA and ConA, but not PWM stimulation. Changes in mitogen responsiveness of experimentally infected Aotus monkeys are similar to those reported for humans with acute falciparum malaria.
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PMID:Effect of falciparum malaria infection on the in vitro mitogen responses of spleen and peripheral blood lymphocytes from owl monkeys. 9 58


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