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

Thymus, spleen, and bone marrow of 1-month-old neonatally Moloney murine leukemia virus-inoculated mice have been transferred to 400-R-irradiated syngeneic recipients of the opposite sex. The donor or recipient origin of T-cell lymphomas arising in the host animal was identified by the sex chromosome marker. Spleen and bone marrow of athymic BALB-nu/nu mice contain cells with the potential to develop into T-cell lymphomas upon transfer to thymus-bearing BALB/c recipients. Such lymphomas arise from at least two subsets of T-cells, one terminal deoxynucleotidyl transferase (TdT) positive and the other 20 alpha-hydroxysteroid dehydrogenase positive. The enzyme-negative precursor T-cells from the BALB-nu/nu spleen and bone marrow can thus mature to enzyme-positive cells and give rise to lymphoma in the thymus-bearing recipient. Preleukemic spleen and bone marrow, but not thymus, from CBA and BALB/c mice regularly contained cells with the potential to develop lymphoma. The subset of T-cell involved was influenced by the genotype since lymphomas arising after the transfer of CBA and BALB/c spleens were TdT positive and 20 alpha-hydroxysteroid dehydrogenase positive, respectively. In thymus-bearing mice, but not in nude mice, the transfer of preleukemic spleen cells gave lymphomas earlier than did transfer of bone marrow cells. This suggests that the more mature lymphoid cell population in the spleen of thymus-bearing mice may allow leukemic transformation to occur more rapidly than do the less mature cells in the bone marrow. In one-third of the cases, the virus produced by the preleukemic cells transferred induced new lymphomas involving recipient host cells. These de novo-induced lymphomas were all TdT positive. We suggest that leukemic transformation of TdT-positive cells may occur through a different mechanism than does transformation of cells bearing the 20 alpha-hydroxysteroid dehydrogenase marker.
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PMID:Influence of genotype and the organ of origin on the subtype of T-cell in Moloney lymphomas induced by transfer of preleukemic cells from athymic and thymus-bearing mice. 387 60

Spleen cells from Lewis rats were cultured with 4 micrograms/ml Con A. These cells were then fused with BW 5147 mouse T lymphoma cells. Two hybrid clones (6B2-B8 and 6B2-E6) obtained by fusion formed CGF effectively. It was found that hybrid cells can be boosted to produce higher levels of CGF upon stimulation with Con A. 6B2-B8 express rat T cell markers. CGF formed by 6B2-B8 had a m.w. of 23,000 and 40,000. CGF was eluted from a Mono Q anion-exchange column with an FPLC system at 0.4 to 0.6 M NaCl as a major peak and at 0.8 M NaCl as a minor peak. CGF was eluted as three peaks with pH 4.1, 4.8, and 5.2 from a Mono P chromatofocusing column. CGF from 6B2-B8 does not contain IL-1, IL-2, IL-3, or CSF.
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PMID:Establishment of rat-mouse T cell hybridomas that constitutively produce a soluble factor that is needed for the generation of cytotoxic cells: biochemical and functional characterization. 387 81

Spleen cells from C.B- 17 scid mice with severe combined immunodeficiency disease exhibit natural killer cell (NK) activity against YAC lymphoma targets in a standard 4-hr 51Cr release assay. The cytolytic activity is demonstrable only at high effector to target ratios but can be augmented at least sevenfold by the interferon inducer poly I:C. The pattern of target lysis is specific, because splenocytes from poly I:C-primed C.B-17 scid mice lyse NK-sensitive YAC cells and not the insensitive P815 mastocytoma. The presence of several NK-associated antigens on C.B-17 scid splenocytes was tested by pretreating cells with the appropriate antiserum plus complement before testing for NK activity. The results indicate that a proportion of NK effectors in C.B-17 scid mice bear surface NK 2.1 and Asialo GM1 but are negative for Thy-1.
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PMID:Natural killer (NK) cells are present in mice with severe combined immunodeficiency (scid). 398 96

In vitro cultures of spleen cells (S) from normal 8-10-wk-old DBA/2J mice were shown to develop a small number of plaque-forming cells (PFC) that released antibodies lytic to syngenic and autologous thymus cells as well as to syngenic lymphoma L5178Y cells used as the target in the PFC assay. A marked increase in the number of PFC detectable on L5178Y target cells was demonstrated on day 4 in the cultures of S cells to which syngenic or autologous thymus cells had been added (S+T) at time 0, whereas the PFC detectable on thymus cells in such cultures remained at a level similar to that in S cultures. This suggested that two populations of PFC participated in the observed phenomena. No PFC developed in the culture of thymus cells (T). The addition of the cell-free supernatants of 24-h cultures of T or of L5178Y cells to syngenic S cultures also caused a specific increase in the number of the PFC detectable on L5178Y, which suggested that certain immunogenic factors released from the T cells stimulated the response observed in the S+T cultures. Antibodies of IgM nature were detected in the supernatants of S+T cultures by means of cytolysis in agar of L5178Y cells. Although such antibodies did not cause lysis of thymus cells, they could be completely removed by absorption with normal adult or fetal thymus cells of syngenic origin. Still, the absorbing capacity of L5178Y was much higher than that of thymus cells. The absorption was more efficient at 4 degrees C than at 22 degrees C, and hardly any absorption occurred at 37 degrees C. The tissue distribution of the antigen under study seemed to be restricted to thymus cells since no other murine tissue cells tested removed the antibodies. The thymic antigen under study was not restricted to strain DBA/2J and could be demonstrated on thymus cells of all other strains tested. On the other hand, the ability of spleen cells to respond in vitro to this antigen has thus far been observed only in DBA/2J mice. Spleen cells of strains C57BL/6J and NZB/BINJ as well as (DBA/2 x NZB)F(1) failed to show any significant increase in the PFC response detectable on the L5178Y target when syngenic thymus cells or DBA/2J thymus cells were added. An intravenous injection of syngenic thymus cells to DBA/2J mice also caused the appearance in their spleens of PFC detectable on the L5178Y target. The described in vitro system may provide a good means of studying the cellular basis of generation of self-tolerance and of its breakdown.
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PMID:In vitro studies on strain-dependent production of thymus-specific autoantibodies. 457 17

C.B-20 mice were immunized with splenocytes or B leukemia cells (BCL1) from Ig H chain allotype congenic strains. Spleen cells from these immunized mice were rechallenged in vitro to generate H-2-restricted cytotoxic T cells that were specific for target antigens controlled by genes linked to the Ig H chain locus. The anti-Ig H cytotoxic T cells detected an antigen(s) expressed only on surface Ig+ cells. Thus, T cell lymphoblasts, eight BALB/c myeloma cell lines, and a T cell lymphoma were not lysed by the effector cells. In contrast, B cell lymphoblasts and the surface Ig+ BCL1 cells were sensitive to lysis. A surface Ig- hybridoma (which secretes the IgM from the BCL1 cells) generated by fusing BCL1 cells to X63 myeloma cells was not killed by the effector cells. These data indicate that cytotoxic T cells specific for antigenic determinants on either surface IgM+ or IgD+ or on a molecule that is coordinately expressed on IgM+ or IgD+ cells can be generated and that such cells might play a role in regulating the growth of normal B cells or surface Ig+ tumor cells in vivo.
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PMID:Cytotoxic T cells specific for antigens expressed on surface immunoglobulin-positive cells. 617 Jul 17

Spleen cells from pregnant and lactating BALB/c mice were depressed in their cytolytic capabilities after in vivo immunization with the allogeneic EL4 lymphoma. However, in vitro spleen cells from both syngeneic (BALB/c X BALB/c) and allogeneic (BALB/c X C57BL/6J) matings responded with proliferative and cytolytic responses which were comparable to virgin controls. Upon secondary in vitro stimulation, in vivo primed maternal cells had responses which were similar to virgin controls. In addition, the in vivo sensitized maternal spleen cells adoptively immunized in irradiated allogeneic recipients responded like the virgin controls. In these studies, suppressor cells could not be detected in either nonimmune or immune maternal spleen cell populations.
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PMID:An in vitro and in vivo analysis of murine immunocompetence during pregnancy and lactation. 621 68

Genetic resistance to Marek's disease in RPL line-6 chickens is expressed not only at the level of host immunological responses against virus an tumour antigens, but also at the level of target lymphoid cells for virus infection and transformation. The nature of the target cell involved was investigated. Spleen cells from susceptible line-7 chickens adsorbed more Marek's disease virus and turkey herpesvirus in vitro than line-6 spleen cells. In the case of Marek's disease virus this was reflected in the replicative ability of the virus in vivo. Transplantation of thymus fragments from 1-day-old line-7 chickens into thymectomized line-6 chickens conferred a high degree of susceptibility on the latter, but the transplantation of spleen or fragments had no significant effect. The reverse procedure, i.e. grafting of line-6 thymi into line-7 chickens, did not diminish the susceptibility of the recipients. In each treatment group the observed titres of leukocyte-associated viraemia correlated with the susceptibility of the group to Marek's disease. Histologically the grafted thymus fragments became depleted of lymphocytes immediately after transplantation. By 6 days there was substantial recovery, apparently as a result of re-population of the thymic epithelium by host stem cells. This was confirmed by transplanting thymus fragments between individuals of opposite sexes. Karyotype analysis showed that the thymus contained lymphocytes of the sex of the recipient. However, karyotype analysis of lymphoma cells taken from recipient line-6 chickens that had received thymus grafts from line-7 birds of the opposite sex showed that, in the majority of cases, the lymphomas consisted of cells of donor origin. It is concluded that the susceptibility of line-7 chickens is largely attributable to the greater susceptibility of their T-lymphocytes to infection and transformation by Marek's disease virus, and that this susceptibility can be transferred to genetically resistant line-6 birds by adoptive transfer of the cells in the form of thymus fragments.
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PMID:The mechanism of genetic resistance to Marek's disease in chickens. 627 8

Spleen cells from mice immunized with Epstein-Barr virus-transformed lymphoblastoid cells (EB-LCL) were used to generate monoclonal antibodies to cell surface antigens associated with the EB virus-transformed state. Radioimmune and immunofluorescence binding assays identified two antibodies, MHM6 and AC2, which reacted consistently with all EB-LCL tested, with a subpopulation of cells in some but not all EB virus genome-positive Burkitt lymphoma lines, but with none of a range of EB virus genome-negative cell lines of lymphoma or leukaemia origin. While MHM6 appeared to bind an EB virus-related antigen, AC2 bound some other cell surface antigen which was also found on a small subpopulation of cells in lymphocyte cultures stimulated with phytohaemagglutinin or with pokeweed mitogen. MHM6 and AC2 recognized single polypeptides with apparent molecular weights of 45 kd and 80 kd respectively as shown by sodium dodecylsulphate polyacrylamide gel electrophoresis (SDS-PAGE) analysis of 125I-labeled cell surface polypeptides immunoprecipitated with these antibodies. These polypeptides were induced on experimentally-infected B cells within 24 h of the expression of the EB virus nuclear antigen, EBNA, at a time known to coincide with the appearance of the lymphocyte-detected membrane antigen, LYDMA. However, saturating concentration of MHM6 and AC2 were unable to protect EB-LCL target cells from lysis by LYDMA-specific cytotoxic T cells in a chromium-release assay.
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PMID:Monoclonal antibodies to Epstein-Barr virus-induced, transformation-associated cell surface antigens: binding patterns and effect upon virus-specific T-cell cytotoxicity. 628 62

Spleen cells from mice infected with the protozoan parasite Encephalitozoon cuniculi demonstrated enhanced in vitro cytolysis of YAC-1 lymphoma cells. Selective cell depletion experiments showed that the dominant cell population mediating cytolysis of YAC-1 tumor cells expressed the characteristic phenotype of murine natural killer (NK) cells because (i) pretreatment of spleen cells with anti-asialo GM 1 antiserum plus complement abolished the cytotoxic activity; (ii) augmented cytolysis was found in athymic nude mice; (iii) pretreatment of spleen cells with anti-Thy 1.2 plus complement did not affect the level of cytolysis; and (iv) nylon wool removal of adherent cells did not reduce the augmented cytolysis. The augmented cytolysis peaked 7 days after infection, gradually diminished, and finally returned to control levels by 21 days postinfection. The parasite-induced augmentation of NK cell activity was dose-dependent: inoculation of 10(7) parasites gave maximum enhancement, whereas 10(5) or 10(4) parasites had an insignificant effect on spontaneous NK cell cytolysis. The augmented NK cell cytotoxicity was dependent upon viable parasites; inoculation of killed parasites failed to stimulate a significant increase in spontaneous cytolysis. An active infectious process was an important component of this process. The peak of NK activity in euthymic mice was closely correlated with the active stage of infection, and reduction of NK cell activity coincided with recovery from infection. By contrast, athymic nude mice were unable to control E. cuniculi infections yet maintained persistently elevated NK responses. The present data, along with previous reports, indicate that infection with E. cuniculi evokes transient modulation of host immune functions.
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PMID:Enhanced natural killer cell activity in experimental murine encephalitozoonosis. 640 1

(C57BL/6 X DBA/2)F1 hybrid (B6D2F1) mice resist the growth of parental-strain (B6) EL-4 lymphoma cells inoculated intraperitoneally; that is, B6D2F1 mice survive longer than B6 mice and do not develop ascites. As compared with B6 mice, B6D2F1 mice have higher levels of natural killer (NK) activity against 51Cr-labelled EL-4 cells in their lymphoid organs. B6D2F1 mice treated with 89Sr lose NK activity for certain lymphoma cell targets, e.g. YAC-1, but NK(EL-4) function is usually intact. However, 89Sr-treated mice had lost hybrid resistance to EL-4 cells in vivo, as determined by survival by irradiated or unirradiated EL-4 cells, Corynebacterium parvum, or polyinosinic:polycytidylic acid (pI:pC) in spleens of normal B6D2F1 mice, but NK(EL-4) activity was depressed within 3 days by such treatment in B6D2F1 mice previously injected with 89Sr. Suppressor cells for NK(EL-4) but not for NK(YAC-1) effectors were easily detected in spleens of 89Sr-treated mice "challenged' with C. parvum. Thus, agents capable of stimulating NK cell function in normal mice may lead to suppression of that activity in mice depleted of marrow-dependent cell function by 89Sr. Spleen cells of 89Sr-treated B6D2F1 mice were also unable to generate anti-EL-4 cytotoxic T lymphocytes in a cell-mediated lympholysis system; this defect appeared also to be mediated by suppressor cells. Lymphoid cells depleted by 89Sr-induced marrow aplasia may have two functions in host defences against tumours (especially lymphomas): they may lyse tumour cells directly and they may "down-regulate' suppressor cells capable of inhibiting other "natural' or "induced' immune functions.
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PMID:Hybrid resistance to EL-4 lymphoma cells. II. Association between loss of hybrid resistance and detection of suppressor cells after treatment of mice with 89Sr. 645 78


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