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)

BCNU treatment of advanced LSA lymphoma, a poorly antigenic tumor of syngeneic C57BL/ym mice, produced large numbers of cured mice which were highly immune against further LSA tumor challenges. Spleen cells from cured mice were transferred into normal naive mice in close temporal relationship to the injection of 10(3) LSA cells and showed that during a period of two days before to one day after tumor injection, the MST and per cent tumor takes could be greatly modified. Activity was only weakly present in bone marrow or thymus cells but mixtures of these cells with or without added spleen cells were effective. In 400 rad sublethally irradiated mice it was also found that transferred spleen cells prevented progression of tumor, and resistance was permanent. This indicates that all elements of tumor recognition, affector and effector limbs of immune response were present in the adoptively transferred spleen cell population.
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PMID:Adoptive transfer of immunity by spleen cells from LSA-lymphoma mice cured by BCNU. 647 99

Studies have shown that there is an abnormality in the thymus of dystrophic mice with respect to age-dependent thymus weight changes and altered morphology (T. DeKretser and B. Livett, Nature (London) 263, 682, 1976). Recently, others have shown that natural killer (NK) cells can lyse cells of a large, immature, rapidly dividing cell subpopulation within the thymus of normal young (3 weeks of age) mice (M. Hansson, K. Karre, R. Kiessling, J. Roder, B. Anderson, and P. Hayry, J. Immunol. 123, 765, 1979). The NK susceptibility of dystrophic mouse thymocytes as targets was therefore studied. Spleen cells from normal (+/+) and dystrophic (dy2J/dy2J) male C57BL/6J mice 8-10 weeks old were passed over nylon wool and the nonadherent cells were incubated with 51Cr-labeled YAC-1 lymphoma target cells or thymocytes in a 51Cr-release assay. Spleen cells from dystrophic mice killed twofold more YAC-1 target cells than did spleen cells from normal mice. Thymocytes from 3- to 4-week-old dystrophic mice were three to four times more susceptible to NK lysis by dystrophic mouse spleen cells as compared with normal mouse spleen cells. Spleen cells from dystrophic mice had the same NK activity against dystrophic and normal mouse thymocytes as targets. Normal mouse spleen cells killed three- to fourfold more dystrophic mouse thymocytes than that of normal mouse thymocytes as targets. Target cell-binding studies revealed that conjugate-forming cells from nylon nonadherent dystrophic mouse spleen cells were found to be two- to fourfold greater than for normal mouse spleen cells using YAC-1 tumor cells as targets. The number of lymphocytes bound per YAC-1 target cell ranged from 2 to 5 for dystrophic mouse spleen cells as compared with 1 to 2 for the normal control group. Using both normal and dystrophic mouse thymocytes as targets, the conjugate-forming cells from dystrophic mouse spleen cells were also found to be twofold greater than in the normal control group. Cold target inhibition studies revealed that the natural killing of dystrophic mouse thymocytes was due to a YAC-1-reactive NK cell. Effector cell depletion studies using monoclonal anti-Thy-1.2 plus complement treatment and plastic petri dish adherence also revealed that the natural killing of dystrophic mouse thymocytes was not due to either T lymphocytes or macrophages. Taken together, these results show an increase in NK-sensitive thymocyte targets in dystrophic mice, in combination with an increase in splenic NK activity.
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PMID:Enhanced natural killer (NK) cell activity and NK-sensitive thymic cells in murine muscular dystrophy. 665 89

The influence of a vitamin C regimen, 250 mg% in the drinking water, on natural killer (NK) cell activity was investigated in three highly inbred strains of mice. Spleen effector cells from these donors, both tap water control and experimental after 4-5 weeks, were tested against YAC-1 murine lymphoma target cells in a 4-hour 51Cr release assay. Ascorbate treatment was observed to be without effect on NK activity in the autoimmune- and lymphoma-prone NZB strain as well as in the normal and low cancer-incidence BALB/c and DBA/2. The relative levels of hemopoietic stem cells, purported to be decisive in determining NK levels, were of a similar order in these three strains as their relative NK activities. It appears that the established association of vitamin C with modulation of the immune response, as observed in activation of T cell-mediated immunity and the enhancement of interferon production, would not include alterations in natural cytotoxic reactivity.
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PMID:Vitamin C and immunity: natural killer (NK) cell factor. 688 75

The ability of thimerosal-killed Blastomyces dermatitidis yeast cells, which greatly enhance the cell-mediated immune response in C57BL/6J mice, to act as an immunopotentiator against EL 4 lymphoma was investigated. Mice treated with yeast cells were protected from as many as 10(4) tumor cells. Complete suppression of tumor growth was observed in treated animals that received ip injections of 10(2) or 10(3) tumor cells. The mice, however, were not immune to further EL 4 lymphoma cell challenge. The lack of tumor-specific immunity indicated nonspecific suppression of tumor growth probably by macrophages. Ten days after treatment, the peritoneal macrophages from mice that showed complete tumor suppression were tested for their ability to prevent in vitro tumor cell proliferation. These macrophages demonstrated 90% inhibition of [3H]thymidine incorporation by EL 4 tumor cells at a 100:1 effector-to-target cell ratio. Macrophages from B. dermatitidis-treated animals exhibited a twofold increase in specific lysis of EL 4 at 10 and 15 days compared to resident macrophages. Spleen and lymph node cells from protected animals showed no cytotoxic activity against EL 4 in a 51Cr release assay. Treatment of tumor-bearing mice with a single dose of B. dermatitidis was effective only if administered within 24 hours of tumor establishment. These results demonstrated that nonviable B. dermatitidis prohibits the growth of EL 4 under conditions where Corynebacterium parvum fails to do so.
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PMID:Immunoadjuvant effects of Blastomyces dermatitidis against EL 4 lymphoma in C57BL/6J mice. 695 9

Cytotoxic T-cells (CTL) could not be detected in spleen cell suspensions from Moloney murine sarcoma virus (M-MuSV)-induced tumor-bearing A/Sn and (A/Sn X C57BL/6) F1 mice, with the A/Sn-derived natural killer (NK)-sensitive YAC-1 lymphoma cells used as targets. However, spleen T-cells from tumor-bearing (A/Sn X C57Bl/6)F1 mice were efficient killers against C57BL/6-derived RBL-5 cells. When tested for viral antigens by sera from mice with regressing atumors, YAC-1 and RBL-5 cells cross-reacted. The anti-RBL-5 effect of spleen cells from A/Sn X C57BL/6)F1 tumor bearers was blocked in cold target competition experiments by YAC-1 cells, which suggested the expression of a CTL target structure on YAC-1 cells. The activity against YAC-1 cells in spleen suspensions of both tumor-bearing and control (A/Sn X C57BL/6)F1 mice seemed to be an NK phenomenon entirely, because blocking occurred neither with RBL-5 cells nor with freshly prepared YAC lymphoma cells, both of which have low sensitivity to NK effects. Spleen cells from (A/Sn X C57BL/6)F1 regressors were stimulated to a secondary CTL response in vitro by YAC-1 and RBL-5 cells, which further indicated that YAC-1 cells express the M-MuSV-specific CTL target structure. These experiments also showed that YAC-1 cells could be lysed by CTL. YAC-1 cells did not induce a secondary response in A/Sn regressors, which indicated a lack of M-MuSV-induced CTL memory cells in this strain. The result was not due to a general unreactivity of A/Sn mice against YAC-1 cells, because spleen cells from YAC-1-immunized mice exhibited strong T-cell-mediated anti-YAC-1 activity after in vitro cultivation. Thus tumor regression seems to occur without the production of CTL in A/Sn mice.
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PMID:Defective cytotoxic T-cell generation in Moloney murine sarcoma virus-infected A/Sn mice. 696 72

Backcross SJL x (SJL x BALB/c)F1 and (SJL x BSVS)F1 mice were examined for their ability to support growth of transplantable SJL lymphoma (reticulum cell sarcoma (RCS). A marked linkage to H-2 was noted in that H-2s/d backcross mice failed to support tumor growth, while H-2s/s backcross mice showed approximately 70% of the growth seen in SJL mice, as judged by lymph node and spleen weights. Spleen cells obtained from backcross mice by splenectomy were examined for their ability to give proliferative responses to gamma-RCS cells, whereafter individual splenectomized mice were also examined for their ability to support lymphoma growth. Both properties showed a similar degree of linkage to H-2 and to each other, although there seemed to be a segregating non-H-2 BALB gene which also exerted an additional, less marked negative influence on the proliferative responses. It is suggested that the proliferative response in vivo may contribute to the lymphoma growth and that the presence of H-2d is inhibitory. (SJL x BSVS)F1 mice gave excellent proliferative responses and supported growth of RCS to approximately 80% of those of controls. These results confirm previous conclusions on the negative effect of H-21d in F1 hybrids on both phenomena.
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PMID:Growth of SJL/J-derived RCS as related to its ability to induce T cell proliferation in the host. II. Negative influence of H-2d1. 703 67

The T-cell enzyme markers, terminal deoxy-nucleotidyltransferase (TDT) and 20 alpha hydroxysteroid dehydrogenase (20 alpha SDH), were used to classify lymphomas induced by the Moloney leukemia virus (M-MuLV). Different subtypes of T cells were shown to be involved in different types of lymphoma. Thymomas were TdT-positive and grew as subcutaneous solid tumors at the site of inoculation. Spleen cells from mice with generalized lymphoma were of two types. In the majority of cases the lymphomas consisted of 20 alpha SDH-positive cells that homed to spleen and lymph nodes upon transplantation. In a few cases the cells of enlarged spleens were TdT-positive and, like the TdT-positive thymomas, could be transplanted as subcutaneous tumors. Thus, TdT-positive and 20 alpha SDH-positive T-cell lymphomas can be distinguished by their homing properties. Preleukemic thymus cells from M-MuLV inoculated mice can, after transfer to 400 -R irradiated syngeneic hosts, induce new lymphomas by virus release or grow in an autonomous fashion in the recipients. Whether of donor or recipient type, these lymphomas are TdT-positive. In contrast, preleukemic bone marrow cells give lymphomas of donor type which are as heterogeneous for T-cell enzymes as are lymphomas induced by neonatal inoculation of M-MuLV.
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PMID:Different T-cell subtypes are associated with pathologically distinct forms of Moloney leukemia virus (M-MuLV)-induced lymphoma. 703 58

The anticancer agent 1,3 Bis(2-chloroethyl)-1-Nitrosourea (BCNU) cures the advanced syngeneic LSA lymphoma of C57BL mice with high efficiency. The cured animals resist further tumor challenge by large numbers of viable syngeneic tumor cells. Growth assays of spleen proliferation of the intravenously inoculated tumor revealed a progressive-regressive pattern of spleen growth after LSA-tumor injection. Lymphoma colony forming units (LCFU) in the spleen initially increased then regressed. In vitro assays of serum showed a lack of cytotoxic activity in mice cured by BCNU. Added spleen, thymus, or bone-marrow cells were similarly ineffective. Spleen and bone-marrow cells from immune mice passively transferred to normal mice showed weak cytotoxic activity against the LSA tumor. BCNU-cured mouse cells were more effective in protection than those cured with Chlorozotocin (CLZ).
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PMID:Evidence for host resistance in 1,3 bis(2-chloroethyl)-1-nitrosourea treatment induced in syngeneic LSA lymphoma. 709 33

The distribution of in vitro-stimulated immune lymphocytes in tumor-bearing mice was studied. Spleen cells from BALB/c mice which had regressed Moloney murine sarcoma virus (M-MSV)-induced primary tumors, were sensitized in vitro by using Moloney murine leukemia virus-induced BALB/c lymphoma (LSTRA). Lymphocytes obtained 6 days after stimulation were examined for cytotoxic activity against LSTRA cells, labeled with 51 Cr or 99mTc, and inoculated into mice bearing MSv-induced primary tumors. The distribution of 52Cr-labeled lymphocytes was determined by counting the radioactivity of each organ. Compared to normal lymphocytes, in vitro-stimulated lymphocytes accumulated significantly in tumor tissues and lymphatic organs. The accumulation of MSV-immune lymphocytes in tumor tissues was not evident in 3-methylcholanthrene-induced BALB/c fibrosarcoma, suggesting the operation of specific mechanisms of accumulation of immune lymphocytes. Scintigraphy was performed by inoculating the 99mTc-labeled lymphocytes via the tail vein the tumor-bearing mice. Visualization of the tumor was possible in mice given in vitro-stimulated lymphocytes.
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PMID:Distribution of in vitro-stimulated immune lymphocytes in mice bearing Moloney murine sarcoma virus-induced primary tumor. 727 51

The effects of the polyribonucleotide interferon inducers, BRL 5907 and BRL 10739, on the spontaneous cytotoxicity of CBA mouse cells towards the allogeneic lymphoma EL-4, were investigated. Intravenous administration of BRL 5907 and BRL 10739 increased the cytotoxic activity of a non-adherent, theta-negative, surface immunoglobulin-negative cell present in the spleen, but had no effect on cells in the lymph nodes. Spleen cell cytotoxicity was established within 24 h of injection of the polyribonucleotides, but had disappeared by 4 days. In addition, injection of mice with BRL 10739 increased the spontaneous cytotoxicity of a nylon-wool-adherent, theta-positive spleen cell. Intraperitoneal injection of mice with BRL 5907 and BRL 10739 also enhanced the cytotoxic activity of a non-adherent peritoneal exudate cell.
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PMID:Spontaneous cytotoxicity of murine cells treated with the interferon inducers BRL 5907 and BRL 10739. 738 Apr 65


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