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

Minor lymphocyte-stilulating (MIs) coded non-H-2-linked lymphocyte-activating determinants (LADs) are present on a late developing subpopulation of murine B lymphocytes. Spleen cells derived from CBA/N mice, a strain with an X-linked defect in B cell function, failed to stimulate a response in MIs-defined mixed lymphocyte reactions (MLRs) with H-2 identical CBA/J or C3H/N responder spleen cells. However, both CBA/J and C3H/N spleen cells induced significant responses in CBA/N responder spleen cells. The inability of CBA/N cells to induce an MIs-defined response was not due to the presence of the nonstimulatory MIsb genotype, since spleen cells of immunologically normal F1 mice derived from crosses of CBA/N and C3H/N mice were stimulatory in MLRs for C3H/N responder cells. Immunologically abnormal CBA/N female x C3H/N male) F1 male mice, which are hemizygous for the CBA/N X chromosome, were also unable to induce a response in MIs-defined MLRs. Although the MIs coded LADs are not X linked in immunologically normal mouse strains, these data indicate that the failure of CBA/N mice to functionally express the MIs-coded LADs is X linked. This characteristic was not secondary to the presence of suppressor cells and is most likely related to the absence of a late developing (mature) subpopulation of B lymphocytes in these mice.
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PMID:Studies on non-H-2-linked lymphocyte-activating determinants. II. Nonexpression of Mls determinants in a mouse strain with an X-linked B lymphocyte immune defect. 6 96

The effect of age on the mitogenic and antigenic responsiveness of B cells is examined in spleen cell cultures of CBA/N and (CBA/N X DBA/2) F1 mice. Spleen cells from young male F1 mice (4- to 6-wk old) show lower mitogenic responses to lipopolysaccharide, a lower frequency of sheep erythrocytes (SRBC)-reactive B-cell precursors, and a lower percentage of Ig-bearing cells than age-matched female F1 mice. The expression of all three functions were found to increase with the age of the F1 male mice. Whereas male F1 mice at 60 wk of age showed an equivalent percentage of Ig-bearing spleen cells and a similar mitogenic responsiveness to LPS when compared to adult female F1 mice, the frequency of SRBC-reactive B-cell precursors remained threefold lower. These findings reveal that there is a slower maturation of B cells in mice expressing the X-linked defect and suggests that the defect has differential effects on the mechanisms of antigen and mitogen activation of B cells.
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PMID:B-cell differentiation in the CBA/N mouse. I. Slower maturation of mitogen and antigen-responsive B cells in mice expressing an X-linked defect. 31 94

Spleen cells from CBA/N mice with an X-linked B cell defect were examined for their ability to form antibody in vitro after stimulation with the T-independent antigen TNP-LPS. In contradistinction to their failure to respond to some conventional T-independent antigens such as type III pneumococcal polysaccharide or DNP-AECM-Ficoll, spleen cells from (CBA/N X DBA/2)F1 male mice were able to make a specific anti-TNP PFC response after culture with TNP-LPS. Their response differed from that of phenotypically normal (CBA/N X DBA/2)F1 female littermate spleen cells in that more TNP-LPS was required to elicit the peak anti-TNP response and the anti-TNP antibody secreted by F1 male cells was of lower avidity than that of F1 female cells. The polyclonal antibody response to unsubstituted LPS did not differ substantially between normal and defective B cells. Tnymus-derived cells were not required for the TNP-LPS response by either F1 male or female cells. We conclude that CBA/NB cells can respond to certain T-independent antigens that are able either to induce a very strong activating signal upon ligand-surface receptor interaction and/or to stimulate immature B cells (with a characteristic high surfact immunoglobulin profile) which fail to respond to antigens like DNP-AECM-Ficoll.
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PMID:In vitro responses of CBA/N mice: spleen cells of mice with an X-linked defect that precludes immune responses to several thymus-independent antigens can respond to TNP-lipopolysaccharide. 78 72

The expression of an X-linked defect in the CBA/N strain of mice has been found to result in a number of immune abnormalities. These include low responsiveness to antigens and a greatly reduced ability to respond to many of the common B cell mitogens. An in vitro manifestation of this condition is the virtual inability of CBA/N B cells to form colonies in lipopolysaccharide (LPS)-containing semisolid agar cultures. In this report we show evidence that the colony-forming ability of CBA/N spleen cells can be effectively restored by the bone marrow stromal-derived cell line S17. Spleen cells from 4-5-week-old homozygous CBA/N female mice were grown in double-layer agar cultures containing S17 feeder layers. Control cultures contained the fibroblast-like cell line 95.17 or were treated with medium alone. It was found that at an input cell concentration of 10(4) cells per plate, CBA/N colony formation was increased from a frequency of approximately 1 in 5,000 to 1 in 50 total splenic cells. Studies with purified surface immunoglobulin-positive cells indicate the direct involvement of S17 in this process. The CBA/N colonies formed were dependent on the presence of a mitogen (LPS) and secreted detectable amounts of IgM. Major implications of these findings and the application of this assay system to study the CBA/N defect have been discussed.
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PMID:The stromal cell line S17 supports the growth of lipopolysaccharide-stimulated CBA/N spleen cell colonies in vitro. 155

Graft-versus-host disease (GVH) was used to induce an autoimmune state in F1 recipients using donor spleen cells, splenic T cells, or Lyt 1+2- splenic T cells from either normal DBA/2 mice or from DBA/2 mice carrying the X-linked immunodeficiency (xid) gene. Recipients were either nondefective (DBA/2 X CBA/N)F1 males or reciprocal cross (CBA/N X DBA/2)F1 male mice carrying the xid gene. GVH induced hypergammaglobulinemia and anti-ssDNA autoantibodies in F1 recipients. Immunodeficient (CBA/N X DBA/2)F1 recipients had less hypergammaglobulinemia and IgG anti-ssDNA than did normal (DBA/2 X CBA/N)F1 recipients. Spleen cells, splenic T cells, and Lyt 1+2- splenic T cells from immunodeficient DBA/2.xid donors were less able to induce GVH and autoimmunity than normal DBA/2 donors. These studies suggest that the xid gene may reduce the autoimmune hyperractive state, but may do so by acting on more than one cell population, including T cells.
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PMID:Effect of the xid gene on graft-versus-host-induced autoantibody production in nonautoimmune mice. 392 60

Mouse spleen cells were stimulated to proliferate in vitro by soluble affinity-purified heterologous antibodies to mouse delta. Antibodies from goat or rabbit antisera to TEPC 1017, a mouse IgD myeloma protein, were purified on an affinity column of TEPC 1033, a second mouse IgD myeloma protein. Maximum uptake of [3H]thymidine in the range of 60,000 cpm was obtained after 48 hr of culture with anti-delta at concentrations of 50 micrograms/ml. In contrast, the hybridoma 10-4.22 anti-delta was nonmitogenic at similar concentrations. The proliferative response was not impaired upon removal of T cells by treatment with an anti-thymocyte serum (ATS), nor by removal of adherent cells by passage of spleen cells over Sephadex G-10 columns and counter-flow centrifugation. Splenic lymphocytes isolated on the fluorescence activated cell sorter (FACS) with intermediate-to-high amounts of surface IgD (sIgD) were responsive to soluble anti-delta, while IgD-negative cells, or cells with low amounts of sIgD, were unresponsive. Spleen cells from mice less than 4 weeks of age, or from mice carrying the X-linked B cell defect (xid), were unresponsive to anti-delta. These results indicate that anti-delta acts similarly to anti-mu in stimulating a proliferative response by later maturing B cells, which are characterized by a high density of sIgD.
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PMID:Activation of mouse lymphocytes by anti-immunoglobulin. IV. Stimulation with soluble heterologous anti-delta antibodies. 642 47

Peyer's patch (PP) and mesenteric lymph node (MLN) cell cultures from young adult X-linked immunodeficient (xid) CBA/N and (CBA/N X DBA/2) F1 male mice support primary anti-sheep erythrocyte (SRBC) plaque-forming cell (PFC) responses, which suggests that gut-associated lymphoreticular tissue (GALT) contains a normal B lymphocyte subpopulation. Further support for this was provided by the observation that PP cells from xid mice gave responses to both TI-1 and TI-2 antigens that were similar to the responses of PP cell cultures from normal mice. Spleen cell cultures from xid mice were unresponsive to SRBC and TI-2 antigens. Proof that GALT of xid mice contain mature B lymphocytes was provided by the demonstration of PP B cells that bear a low density of surface immunoglobulin M. When these cells were separated by flow cytometry and immunized with trinitrophenyl (TNP)-Ficoll in vitro, good anti-TNP PFC responses were observed. These results suggest that GALT of young adult xid mice contain mature B cells and may represent the origin for the mature B cell responses seen in aged xid mice.
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PMID:Evidence for a mature B cell subpopulation in Peyer's patches of young adult xid mice. 660 Apr 93

Surface immunoglobulin on spleen cells from NZB and NZB/W mice and congenic mice bearing the nude or X-linked immune defective (Xid) gene was examined by flow microfluorometry with regard to both the frequency of positive cells and density expressed on the cell. These data indicate that although the frequency of unseparated sIg+ B lymphocytes is equivalent among all of these groups of mice, the densities of sIgM and sIgD are different. Spleen cells from these mice were also separated by free-flow electrophoresis and analyzed in a similar manner. This analysis demonstrated the absence of a subpopulation of B lymphocytes with a low electrophoretic mobility and low expression of sIgM. These studies suggest that maturational and/or activation states of the B cells in mice bearing the Xid or nude genes are different from those seen in the parent strains of mice. Such alterations in cell-surface antigens correlate with the differences in the natural history of immunopathology of the autoimmune disease in these congenic colonies of New Zealand mice.
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PMID:Studies of congenitally immunologically mutant New Zealand mice. VIII. Cell-surface phenotype of spleen cells of Xid and nude mice. 660 87

We describe the identification of a monoclonal antibody that recognizes a determinant on the delta chain of mice of the Iga, allotype groups. The monoclonal Ig in soluble form induces allotype-specific proliferation by splenic B lymphocytes from normal animals of these haplotypes. Spleen cells from mice bearing the X-linked defect of CBA/N mice fail to respond, although they bear the determinant. Proliferation is independent of T lymphocytes. The data indicate a direct triggering function for sIgD.
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PMID:Regulation of murine B cells through surface immunoglobulin. I. Monoclonal anti-delta antibody that induces allotype-specific proliferation. 677 25

Xanthan gum (XG), a microbial polysaccharide produced extracellularly by fermentation of Xanthomonas campestris, has unique physical properties. We studied the effects of XG on murine lymphocytes in vitro and found that XG induced both a significant increase of DNA synthesis in mouse splenic B cells and thymocytes as well as polyclonal IgM and IgG antibody responses in B cells. XG-activated thymocytes, however, did not display helper or suppressor functions. XG was almost as effective in inducing polyclonal antibody responses as lipopolysaccharide (LPS) in murine systems. Hamster spleen cells, however, were weakly triggered to nonspecific antibody production by XG but they were not triggered at all by LPS. Spleen cells from normal neonatal mice and from adult CBA/N mice, a strain which possesses an X-linked defect affecting B cell differentiation, responded relatively well to XG and LPS, suggesting that XG can stimulate immature B cells as well as LPS does. It was found that XG activated B cells in the relative absence of T cells and macrophages. Spleen cells from LPS-nonresponder C3H/HeJ mice and seven other mouse strains were stimulated to polyclonal antibody production by XG. In contrast, spleen cells from C57BL/10 mice were unresponsive or only slightly responsive to XG, but fully responsive to LPS.
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PMID:Immune responses to xanthan gum. I. The characteristics of lymphocyte activation by xanthan gum. 683 12


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