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

Spleen cells of BALB/c mice immunized with purified BALB/c myeloma protein (MP) caused idiotype-specific suppression of DNA synthesis and colony formation by myeloma cells in vitro. Lymphocytes from mice immunized with 315-MP inhibited only MOPC-315 plasmacytoma cells; conversely, lymphocytes from mice immunized with 167-MP inhibited only MOPC-167 plasmacytoma cells. Antisera from those mice that showed cell-mediated inhibition of myeloma growth had no significant effect. The suppressive activity of the spleen cells was markedly reduced by treatment with anti-Thy 1.2 and complement, and the immune cells responsible for the suppression did not adhere to nylon wool. The suppressor cells adsorbed to myeloma protein-coated plates, and after elution, inhibited myeloma cells specifically at a 1:1 effector to target cell ratio. Suppression of myeloma growth was due to cytostatic rather than cytolytic effects. These findings suggest that mice immunized with purified myeloma protein have idiotype-specific T cells that can regulate myeloma cell growth. This mechanism may provide an explanation for the transplantation resistance to myelomas induced by immunization with myeloma protein. Similar idiotype-specific T cells may also play a role in the idiotype-specific regulation of immune responses by acting late in differentiation to block the proliferation of antibody-secreting normal B cells.
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PMID:Regulation of myeloma growth in vitro by idiotype-specific T lymphocytes. 696 96

This study demonstrated that spleen cells of inbred BALB/c mice with plasmacytomas inhibited proliferation of the B-lymphocyte colony-forming cells that were precursors of immunoglobulin-producing cells. The number of B-lymphocyte colonies/10(5) nucleated spleen cells was depressed in mice with plasmacytomas. The degree of suppression correlated with the size of the tumor. Spleen cells from tumor-bearing mice suppressed the formation of B-lymphocyte colonies by normal BALB/c spleen cells. Treatment of the myeloma spleen cell suspensions with anti-immunoglobulins, anti-theta, or 1,500 rads did not prevent the suppression. Spleen cells from tumor-bearing mice depleted of adherent cells by passage over Sephadex G-10 columns or adherence to plastic dishes did not retain their suppressive activity. Adherent spleen cells inhibited B-lymphocyte colony formation when they were either in direct contact with normal spleen cells or separated from them by a layer of agar. These studies suggested that the immune suppression seen in plasmacytoma-bearing mice occurred partially at the level of the B-lymphocyte progenitor cell and that this suppression was mediated by an adherent mononuclear cell.
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PMID:Inhibition of B-lymphocyte clonal proliferation by spleen cells from plasmacytoma-bearing mice. 696 47

The present study investigates the fate of effector T cell population against tumor-associated transplantation antigens (TATA) of X5563 plasmacytoma in syngeneic mice rendered specifically unresponsive to the TATA. In this tumor system T cell-mediated tumor-specific immunity was induced by intradermal inoculation of viable tumor cells followed by the surgical resection of the tumor (immunization procedure). The intravenous (iv) presensitization of syngeneic hosts with X-irradiated tumor cells abolished the capability of those hosts to develop the tumor-specific immunity after the above appropriate immunization procedure. Spleen cells from the pretreated mice which subsequently received the immunization procedure could not regain the tumor-neutralizing activity after enzymatic treatment with papain. Moreover, lymphoid cells from the pretreated mice could not be stimulated by the immunization procedure even after proteolytic treatment with papain or trypsin, followed by transfer into other recipient mice free of the serum suppressive factor(s). On the other hand, such enzyme treatment was capable of preventing the tolerance induction of dinitrophenyl (DNP)-primed B cells after in vitro pulsing with DNP-D-GL (copolymer of D-glutamic acid and D-lysine) for 2 hr, suggesting that the enzymatic treatment used here was adequate to remove the blocked receptor and any tolerogen. These results suggest that in X5563 plasmacytoma system, the above specific unresponsiveness induced by the iv presensitization with TATA is due to the irreversible inhibition or deletion of effector T cell clones rather than mere effector cell blockade.
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PMID:The mechanism of specific suppression in effector T cell clones against tumor-associated transplantation antigens. 703 82

Spleen leukocytes from rats and mice immunized against mouse 2.5S nerve growth factor (NGF) and peripheral blood leukocytes from rabbits hyper-immunized against the same antigen were fused with the mouse plasmacytoma P3X63Ag8. Hybridomas were screened by immunological assays (micro-complement fixation test and solid phase radioimmunoassay) for production of antibodies that reacted with NGF. Significant variations were seen between culture fluids from different hybrid cells. In addition, most but not all hybridoma antibodies that reacted immunologically with NGF prevented neurite outgrowth from 8-day chick embryo sensory ganglia explants after binding to NGF. These results suggest that the hybridoma antibodies produced by the different clones react with different antigenic sites on the NGF molecule.
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PMID:Monoclonal antibodies against mouse nerve growth factor produced by somatic cell hybrids. 721 74

Some parameters of the Winn assay for the detection of tumor-suppressing ("effector") and tumor-enhancing lymphoid cells were studied in BALB/c mice. Spleen cells of mice that were preimmunized with mitomycin-C-treated MOPC-104E plasmacytoma cells were inhibitory in this test system for both the MOPC-104E and the HOPC-I plasmacytomas, thus indicating cross-reactivity. Spleen cells taken from mice 6 days after the surgical removal of 15-day-old MOPC-104E tumors inhibited the growth of lethal doses of MOPC-104E cells in normal recipients, but no inhibition was observed 2 days after the removal of 18-day-old tumors. Spleen cells from mice bearing MOPC-104E for 13 days enhanced tumor growth. This enhancement was not influenced significantly by the wide dose range (from 10(5) to 3 x 10(7)) of MOPC-104E cells used to initiate tumors in the lymphoid cell donors, although tendency for stronger enhancing potential occurred after low tumor doses. When spleen cells from donors bearing MOPC-104E for 10 days were injected at the constant tumor-lymphocyte ratio of 1:30 with increasing numbers of tumor cells (from 5 x 10(5) to 2 x 10(6)), tumor inhibition occurred at the lowest dose only, while no significant effect was observed at higher tumor cell doses. When a constant dose (5 x 10(5)) of tumor cells was injected with spleen cells from 10-day tumor-bearers at tumor/lymphocyte ratios of 1:10, u:40 and 1:160, a significant tumor inhibition occurred only at the ratio of 1:40. The relevance of the Winn test to the study of immune mechanisms in tumor-bearing hosts is discussed.
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PMID:Effector and enhancing lymphoid cells in plasmacytoma-bearing mice. I. Methodological studies on the Winn assay. 737 72

Studies were undertaken to produce monoclonal antibodies directed against the murine receptor for macrophage colony-stimulating factor (M-CSF or CSF-1). Sprague-Dawley rats were injected with lysates prepared from a murine myelomonocytic cell line (RAW cell line) that has high levels of M-CSF receptors. Spleen cells from immunized animals were fused with murine plasmacytoma cells and expanded. Supernatants from these cells caused inhibition of 125I-CSF binding to either RAW cells or normal murine marrow cells. Antibody-producing cells were cloned by limiting dilution and by colony growth in agar. The antireceptor antibodies appear specific as they neutralize colony formation by M-CSF but have little or no effect on colony growth in response to the other hemopoietic growth factors granulocyte CSF (G-CSF), granulocyte-macrophage CSF (GM-CSF), interleukin-3 (IL-3) or erythropoietin. These antibodies should aid in defining the role of M-CSF in hemopoiesis in vivo.
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PMID:Preparation of a monoclonal antibody directed against the receptor for murine colony-stimulating factor-1. 846 60

Rat AgB transplantation antigens were isolated after papain digestion of spleens from the inbred strain Hooded Lister. Both subunits of the AgB antigens were present in the purified material. Some physical characteristics of the antigens have been determined. An antiserum, raised in a rabbit, against the purified material reacted exclusively with AgB antigens on splenocytes but detected novel structures on both adult and embryonic fibroblasts. These structures, antigenically related to AgB antigens, were not detected on plasmacytoma or hepatoma cells, nor did they display any antigenic similarity with rat beta 2-microglobulin. Radioimmunoassays specific for the AgB antigen heavy chain and for beta 2-microglobulin, respectively, were used to estimate the contents of these antigens in several tissues. Spleen and thymus exhibit the largest density, while brain is almost devoid of these antigens.
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PMID:Properties of purified papain-solubilized rat AgB antigens and reactivity of a xenoantiserum against the isolated antigens. 953 30


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