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)

The effect of related and unrelated compounds on the specific binding of dinitrophenyl-coupled bacteriophage (DNP-T4) to lymphoid cell receptors has been examined and compared with the effect on the neutralization of DNP-T4 by anti-DNP serum. Spleen cells and sera from Balb/c mice immunized with DNP-bovine serum albumin were used. The binding of DNP-T4 to the cells was inhibited by DNP-eAcp, di-DNP-Lys, DNP-Tyr, DNP-p(Ornith) and DNP-BSA (among the DNP-derivatives tested), TNP-BSA, ARS-p(Tyr) and TGA. In addition with the above named DNP and TNP compounds, the DNP-T4neutralization by antiserum was also prevented by DNP-derivatives with either L-cysteic acid, alanine, glutamine or poly-L-glutamic acid, while ARS-p(Tyr) and TGA were not effective. Plain carriers (BSA, HSA, poly-ornithine, polylysine and polyglutaminc acid) and cell-mitogens (ConA, LPS and PPD) had no significant inhibitory effect. The results obtained indicate the occurrence of differences between cell-bound receptors and circulating antibodies in what concerning their specific reaction with the dinitrophenyl determinant.
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PMID:Inhibition of specific binding of DNP (dinitrophenyl) determinant to lymphoid-cell receptors by related and unrelated compounds : quantitative studies in vitro. 6 Sep 7

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

Spleen cells from normal BALB/c mice showed in vitro proliferative response against hapten-conjugated syngeneic spleen cells. Trinitrophenylated (TNP) spleen cells were prepared by treating normal spleen cells with sodium 2,4,6-trinitrobenzenesulphonate (TNBS). Four-day cultures of TNP-labelled spleen cells incorporated 2.5-7.4 times more [3H]thymidine than similar cultures of untreated spleen cells. An obviously positive mixed lymphocyte reaction (MLR) by normal spleen cells against mitomycin C (MC) treated TNP-labeled syngeneic spleen cells was observed after 4 days of culture. The MLR to TNP-labelled syngeneic cells was inhibited in the presence of epsilon-TNP-L-lysine by 23-37%. The spleen cells from the mice injected intraperitoneally with TNP-labelled syngeneic spleen cells showed a higher MLR against TNP-labelled spleen cells than normal spleen cells. The sensitized spleen cells also showed an increased response to MC-treated spleen cells. These results suggest that normal spleen cells include cells which can recognize the hapten and new antigenic determinants introduced into syngeneic spleen by chemical modification.
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PMID:In vitro proliferative response of BALB/c mouse spleen cells stimulated with trinitrophenylated syngeneic spleen cells. 12 44

Mice exposed to a sublethal dose of X-rays were immunized with alum-precipitated DNP-KLH (dinitrophenyl-keyhole limpet haemocyanin) and B. pertussis either before or after irradiation. The primary anti-DNP antibody response was evaluated during 8 weeks after immunization by the equilibrium dialysis technique using ammonium sulphate- precipitated serum globulins and the ligand 3H-labelled xi-DNP-L-Lysine. The serum concentrations of antibody sites in mice immunized 1-5 days before or 2 h-8 weeks after 450 rad were below the values in unirradiated controls at all bleeding times. Antibody affinity, however, was found to be up to 20 fold higher in irradiated mice than in control mice when antigen was injected before, or 3-8 weeks after, irradiation. Spleen cells from mice exposed to 450 rad 1-9 weeks before killing were stimulated in vitro with PHA, ConA, or LPS. Recovery profiles of mitotic responsiveness suggest that enhancement of antibody affinity in irradiated mice could result from relative lack of suppressor T Cells.
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PMID:Effects of whole-body irradiation on antibody affinity. 19 58

Spleen lymphocytes and erythrocytes from congenic mice of diffrent haplotypes were characterized on a precise biophysical basis (the anodic electrophoretic mobility, EPM) to correlate any subtle differences in the cell surface topochemistry with the H-2 specificity. Spleen T lymphocytes from A.CA (H-2f) and A.SW (H-2s) mice exhibited high values EPM, which were significantly different. In contrast, significant differences in the EPM of B cells and erythrocytes were not observed. Cell electrophoresis of spleen T lymphocytes (without " contaminating " B cells), before and after the chemical modification of the cell surface by treatment with small/non-toxic concentrations of maleic anhydride, showed the number of lysine side chain amino-groups in the periphery of cells with H-2f specificity to be about twice those on cells with H-2s haplotype. Such a difference was observed both in the case of premature T lymphocytes and mature T lymphocytes. The difference in the number of cationogenic amino-groups in the cell periphery contributing a positive charge, would explain the oberved difference in the EPM of H-2f and H-2s spleen T lymphocytes, and suggest that the macromolecules coded by the H-2 genes or other genes under H-2 control lead to delicate differences in the chemical composition of the surface membranes of cells of the two H-2 haplotypes, expressed only on high EPM lymphocytes of spleen (T or T-like cells).
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PMID:[Genetic control of the H-2 region of the cell surface: cationic amino groups in the periphery of T lymphocytes]. 30 May 97

The palmitoyl derivative of the linear polypeptide of poly-(L-Glu-L-Lys-L-Phe)n (GLphi) can be coupled to spleen cells directly. The intravenous administration of 2 X 10(5)--3 X 10(7) GLphi-coupled syngeneic spleen cells induces GL-phi-specific suppressor T cells in C57BL/6 nonresponder mice. The suppression is antigen specific and can be detected by the inhibition of the primary GLphi plaque-forming cell response to challenge with GLphi-fowl gamma globulin. The number of inducer cells required for suppression carry less than 0.1 microgram of antigen. Spleen cells from tolerized mice can transfer suppression to normal syngeneic recipients. The suppression is cyclophosphamide sensitive and the suppressor cells bear the Thy 1.2 marker. This method of inducing antigen-specific suppressor cells may be generally applicable to other antigen systems.
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PMID:Immune suppression in vivo with antigen-modified syngeneic cells. I. T-cell-mediated suppression to the terpolymer poly-(Glu, Lys, Phe)n. 30 20

The susceptibility of mouse spleen cells to hapten-specific tolerance induction of a primary in vitro thymus-independent antibody response was examined. Both the induction of tolerance by 2,4,6-trinitrophenyl-D-glutamic acid-D-lysine (TNP96D-GL) and of antibody formation (elicited by TNP-Brucella abortus) in neonatal spleen cell cultures were unaffected by anti-Thy-1.2 plus complement treatment. Spleen cells from neonatal mice were only slightly more sensitive to TNP96D-GL tolerance induction than were cells from adult mice. The difference in susceptibility to tolerance induction was not nearly as great as that predicted by "clonal abortion"-type theories of B cell tolerogenesis.
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PMID:Ontogeny of susceptibility of mouse splenic B cells to tolerance induction in vitro by TNP-D-GL. 31 1

Anaerobic diphtheroids possessing lympho-reticular stimulatory properties may differ considerably in their peptidoglycan composition. Spleen weight-increasing activity of strains directly parallels their antitumour properties. P. granulosum strains, inactive in assays for lympho-reticular stimulation, appear to have a higher cell wall alanine content than most of the P. acnes and P. avidum strains tested. Two P. acnes strains, however, had equivalently high alanine ratios and were stimulatory. The presence of galactose does not appear to be required for activity since P. acnes II strains which lack this sugar can be fully stimulatory. The existence of the species P. lymphophilum (Torrey) is further supported by the finding of two more serologically identical strains which do not cross react serologically with the other species in the group. These organisms are fully stimulatory but have lysine rather than DAP as their cell wall diamino acid.
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PMID:Comparative studies on the cell wall composition of some anaerobic coryneforms of varying lympho-reticular stimulatory activity. 60 97

Previous studies have demonstrated an inverse relationship between the net electrical charge of immunogens and the antibodies they elicit. This correlation was found to be expressed at the cellular level. It has been shown that thymus-derived cells may recognize immunogens on the basis of their overall electrical charge. In this study, charged T-independent copolymers composed of tyrosine, glutamic acid, and lysine of the D configuration were prepared in order to find out whether this net charge phenomenon holds also for immunogens which do not require helper T cells for generation of immune response. Spleen cells were fractionated over negatively charged glass bead columns, and their immunocompetence was tested by transferring them into irradiated recipient mice which were immunized with the dinitrophenylated acidic or basic T-independent carrier. No differences in the responsiveness to the dinitrophenyl group on either carrier could be detected in recipients of unfractionated or fractionated cells on the charged columns. Similar results were obtained with the negatively charged T-independent branched polypeptide poly-(DTyr,DGlu)-poly(DPro)--poly(DLys). Filtration of spleen cells through glass bead columns did not affect the immune response potential of the recipient mice. In contrast, a significant reduction was observed in the frequency of positive responses in recipients of filtered cells, which were immunized with the negatively charged T-dependent poly(DTyr,DGlu)-poly(DPro)--poly(DLys). Thus, the inverse net charge phenomenon holds only for T-dependent antigens.
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PMID:Lack of inverse relationship between the net charge of T-independent immunogens and the responding spleen cells. 108 Nov 4

Trinitrophenyl (TNP) human gamma-globulin with low-epitope-density tolerizes B cells from normal BDF1 mice in a Fc gamma receptor-dependent manner but does not tolerize B cells from preautoimmune NZB mice. In order to investigate the relationships between tolerance induction and epitope density independently of Fc gamma receptor function in these two strains, TNP conjugates of two additional thymic-independent tolerogenic carriers, D-glutamic acid-D-lysine (D-GL) and carboxymethyl cellulose (CMC), were tested. A brief pulse with low-epitope-density conjugates such as TNP4.4-D-GL rendered unfractionated or T-cell-depleted spleen cells from BDF1 but not NZB mice tolerant in a hapten-specific manner. Spleen cells from NZB mice, however, were susceptible to tolerization with TNP13.5-D-GL. NZB mice were also resistant to tolerance induction in vivo with TNP5.5-D-GL, TNP3-CMC, and TNP6-CMC, all of which tolerize BDF1 mice in vivo. Both strains were tolerized with TNP13.5-D-GL and TNP13-CMC in vivo. NZB mice were also significantly less susceptible to tolerance induction with TNP3-CMC when TNP-Ficoll was substituted for TNP Brucella abortus as the challenge antigen. These findings militate against the possibility that an Fc gamma receptor defect is the principal mechanism of resistance of NZB B cells to tolerance induction with-low-epitope density conjugates.
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PMID:Defective B-cell tolerance in New Zealand black mice. Fc receptor-independence of resistance to low-epitope-density tolerogens. 245 99


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