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)

Immune responsiveness was compared in B6AF1 mice after one, two, three, or four donor-specific DBA/2 blood transfusions (DST). Ten days after the last transfusion, the spleen cells of transfused mice were assayed for direct lymphocyte-mediated cytotoxicity, for the ability to respond in mixed lymphocyte culture (MLC) and cell-mediated lymphocytotoxic (CML) assays to DBA/2 and C3H/He antigens, and for the ability to inhibit the MLC and CML response of normal B6AF1 to DBA/2 and C3H/He antigens. Immune responsiveness was also tested in B6AF1 2 to 80 days after a single DBA/2 DST. The MLC response of transfused mice was specifically suppressed to the blood donor after both single and multiple transfusions. The CML response to DBA/2 was suppressed after a single DST, but returned to normal after multiple transfusions. Spleen cells from transfused mice did not inhibit the MLC response of normal B6AF1 mice to DBA/2 or C3H/He antigens after one or two transfusions regardless of time tested, but were able to inhibit the response to both stimulators after three or more transfusions. The MLC response remained specifically suppressed to the blood donor for as long as 80 days after a single DST, while the CML response was suppressed up to 50 days after transfusion, but had returned to normal by 80 days.
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PMID:Comparison of immune responsiveness in mice after single or multiple donor-specific transfusions. 619 72

Spleen cells from DBA/2 mice that received a single feeding of 20 mg of ovalbumin (OVA) 7 days previously were specifically hyporesponsive to primary in vitro challenge with the thymic-dependent antigen TNP-polymerized ovalbumin (TNP-POL-OVA). The tolerance observed in spleen cells from OVA-fed animals was dependent upon OVA-specific T suppressor cells, because splenic T cells from OVA-fed mice suppressed the primary response to TNP-POL-OVA of cultures containing normal T and B cells. The tolerance and suppression was OVA specific, because spleen cells from OVA-fed animals responded well to other antigens (including TNP on another carrier), and splenic T cells from OVA-fed mice did not affect the response of normal T and B cells to sheep erythrocytes. These data confirm the existence of T suppressor cells after OVA feeding and provide a direct means of assaying their activity in a primary in vitro response.
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PMID:Regulation of the primary in vitro response to TNP-polymerized ovalbumin by T suppressor cells induced by ovalbumin feeding. 623 61

P815 tumor cells (10(7] were administered intraperitoneally to DBA/2 mice. As the ascites tumor grew in the syngeneic host, a decline leading to a total loss of host spleen natural killer (NK) activity could be demonstrated. Removal of T and B cells or macrophages from the tumor-bearing (TB) mouse spleen cells did not raise the level of NK activity. Spleen cells from TB mice did not inhibit the NK activity of normal spleen cells. Comparable target (YAC cells) binding capacity could be demonstrated in spleen cells derived from normal or TB mice, but interferon failed to significantly stimulate the NK activity of TB mouse spleen cells. In adoptive transfer experiments, transfer of spleen or bone marrow cells from TB mice resulted in the development of significant levels of spleen NK activity in lethally X-irradiated recipient DBA/2 mice. These results indicate that the impairment of NK cell differentiation pathway rather than active suppression at the level of effector cells may be the mechanism of loss of NK activity in P815 TB DBA/2 mice.
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PMID:Mechanism of loss of natural killer activity in P815 ascites tumor bearing DBA/2 mice. 623 48

Spleen cells from a DBA/2 mouse immunized with RL male 1 tumor cells, a radiation induced BALB/c T-cell leukemia, were hybridized with the nonsecretor myeloma line NS.1. Four established hybrid cell lines continuously secreted antibodies that recognized a new alloantigenic specificity, tentatively called Ly-m22. This antigen is detectable on nearly 60% of lymph node cells, and 30% of spleen cells by direct cytotoxicity assay, but did not lyse significant number of cells of thymus and bone marrow. By absorption test, these lymphoid organs, i.e., lymph node, spleen, thymus, and bone marrow, were shown to express Ly-m22 determinant. The newly found antigen is expressed predominantly on T-cells. Analysis of BXD and SWXL recombinant inbred strains revealed close linkage between Ly-m22 and Ltw-4 loci on chromosome 1. The estimated recombination frequency is 0.027 +/- 0.081.
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PMID:Mouse alloantigen system Ly-m22 predominantly expressed on T lymphocytes and controlled by a gene linked to M1s region on chromosome 1. 633 54

The effect of cyclosporin A (CsA) on the production of gamma interferon (IFN gamma) versus IFN alpha/beta was studied using mouse and human lymphocytes and fibroblasts. Spleen cells from C57Bl/6 mice produced low but significant levels (40-60 U/ml) of IFN gamma after 2 to 3 days of culture with irradiated DBA spleen cells. The addition of CsA at concentrations as low as 0.1 microgram/ml completely inhibited (less than 10 U/ml) IFN gamma production in these cultures. High levels of IFN gamma (170-1200 U/ml) were produced when either C57Bl/6 spleen cells or Ficoll-Hypaque-purified human peripheral blood lymphocytes (PBL) were cultured with the T-cell mitogen staphylococcal enterotoxin A (SEA). The addition of CsA (0.1 microgram/ml) to these cultures also completely inhibited (less than 10 U/ml) IFN gamma production. This inhibition was shown not to be due to a change in the kinetics of IFN gamma production or to a change in the amount of SEA required for stimulation. IFN gamma production in SEA-stimulated mouse spleen cells was inhibited at 3 days of culture even when CsA was added at 24 or 48 hr postculture initiation. Thus, CsA inhibits IFN gamma production even when early events associated with lymphocyte activation have been allowed to take place. In contrast to IFN gamma production, IFN alpha/beta production by Newcastle disease virus (NDV)-infected mouse and human lymphocytes or fibroblasts was not inhibited by the addition of CsA (1 microgram/ml). CsA also did not block the action of IFN gamma or IFN alpha/beta since addition of CsA (1 microgram/ml) to reference IFN standards had no effect on their antiviral activity. Thus, CsA inhibits the production of IFN gamma by T cells but appears to have no effect on the production of IFN alpha/beta by virus-infected cells or on the antiviral action of already produced IFN gamma and IFN alpha/beta.
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PMID:Cyclosporin A inhibits the production of gamma interferon (IFN gamma), but does not inhibit production of virus-induced IFN alpha/beta. 640 74

Intracameral inoculation of allogeneic P815 mastocytoma cells (DBA/2) into BALB/c mice resulted in progressively growing intraocular tumors. Intraocular tumor cells disseminated rapidly to the spleen and cervical lymph nodes, yet extraocular nests of tumor cells never developed into fulminant tumors. Further experiments showed that tumor cells were continuously seeded from the primary intraocular tumor and were rapidly cleared from extraocular sites. Hosts harboring intraocular P815 mastocytomas rejected tumorigenic doses of P815 cells inoculated subcutaneously or even into the contralateral anterior chamber. This systemic tumor immunity was found to be radiosensitive and T cell dependent. Spleen cells from animals with progressively growing intraocular tumors protected recipient mice challenged with intracamerally inoculated tumor cells and thus suggests that a cell-mediated mechanism is the underlying basis for this form of tumor immunity. The data indicate that mice harboring progressively growing intraocular tumors develop a potent state of "concomitant immunity," that prevents the development of metastases, yet is ineffective in controlling the primary tumor.
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PMID:Intracamerally induced concomitant immunity: mice harboring progressively growing intraocular tumors are immune to spontaneous metastases and secondary tumor challenge. 641 74

Spleen cells from DBA/2 mice immunized with high numbers of sheep red blood cells specifically suppress the primary anti-SRBC antibody response of syngeneic recipients specifically suppress the primary anti-SRBC antibody response of syngeneic recipients after in vivo transfer. Such suppressive activity of the immune spleen cells is mediated by null cells, or by T cells resistant to the cytotoxic activity of anti-Thy 1.2 antiserum plus complement. The primary anti-SRBC antibody response is much higher in NZB mice than in DBA/2 mice, and the suppressive activity of syngeneic immune spleen cells is much lower in NZB than in DBA/2 recipients. Immune spleen cells from DBA/2 donors do not provide more effective suppression than NZB spleen cells in NZB recipients. Conversely, immune spleen cells from NZB donors strongly suppress the anti-SRBC primary response of DBA/2 recipients to the same extent as DBA/2 immune spleen cells. Finally, NZB mice generate specific suppressor cells but their primary antibody response is not sensitive to this suppressor activity.
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PMID:Thymic function in NZB mice. III. Impairment of the activity of specific suppressor cells involved in the regulation of antibody production against sheep red blood cells. 645 Jun 52

Spleen cells of DBA/2 mice bearing subcutaneous implants of the syngeneic tumor L5178Y induce suppression of the in vitro antibody response of normal spleen cells to sheep erythrocytes (SRBC). Cells mediating suppression are detected in the spleens of tumor-bearing mice as early as 24 hr post-implantation but are no longer detected there 15 days post-implantation. These spleen cells are nylon wool nonadherent, sensitive to anti-Thy 1.2 + C and anti-Lyt 1.1 + C, and insensitive to anti-Lyt 2.1 + C treatment. The anti-SRBC response of the unfractionated spleen cells from the tumor-bearing mice is not itself suppressed at the cell numbers used. This along with the finding that suppression occurs in the presence of spleen cells from normal mice suggest that a cell population from the normal mouse spleen is also involved in the suppression. Spleen cells from mice inoculated with irradiated (nonproliferating) L5178Y cells are similarly capable of mediating nonspecific suppression for the same limited period of time after the inoculation. In addition, spleen cells from mice stimulated with several nontumorigenic cellular antigens interact with normal spleen cells to produce suppression. These findings suggest that suppression observed in vitro with spleen cells from these tumor-bearing mice may be the result of antigen-activated cells triggering normal immunoregulatory cells.
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PMID:Evidence for interaction between T cell populations of tumor-bearing and normal mice in immune suppression. 645 72

(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

Spleen cells collected from DBA/2 (H-2d) mice inoculated with the polycythemic variant of Friend-Leukemia Virus Complex (FLV-P) were tested for T-dependent immune functions, such as the in vitro generation of cytotoxic T lymphocytes (CTL) and of non-specific T suppressor lymphocytes (STL). CTL were generated against H-2b splenocytes, and STL were obtained following a 5-day lymphocyte culture without stimulator cells. A progressive and severe impairment of the generation of both CLT and STL was found from 2 weeks onward after infection, being almost totally abolished 3-4 weeks after virus challenge. Suppressor cells (SC) capable of inhibiting CTL generation was detected in FLV-P bearing mice. Suppressor activity was unaffected by anti-Thy 1.2 serum and complement but was removed following iron-magnet depletion or passage through nylon-wool column. Moreover complete recovery of the competence of CTL generation was attained when FLV-P infected splenocytes were passed through nylon-wool column. It is concluded that FLV-P infection depresses T-dependent cytotoxic and suppressor responses in mice, by the appearance of non-T adherent phagocytic cells, capable of impairing CTL generation in vitro.
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PMID:Impairment of in vitro generation of cytotoxic or T suppressor lymphocytes by Friend leukemia virus infection in mice. 645 95


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