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

NK activity in mice is high between about 6 and 10 weeks of age. In contrast, infant mice and mice older than 12-14 weeks of age usually have quite low or undetectable NK activity. Studies were performed to analyze the mechanisms underlying this characteristic age-related regulation of NK activity. Spleen cells from infant mice did not develop appreciable NK activity upon incubation for 12-18 h with either interferon (IFN) or interleukin-2 (IL-2). Analysis of the frequency of IL-2-dependent progenitors of NK cells, in a limiting dilution assay, also indicated that the spleens of infant mice are deficient in precursors of NK cells. In contrast, spleen cells from old mice (30 weeks old) developed substantial levels of NK activity upon incubation with either IFN or IL-2, and they showed a frequency of IL-2-dependent progenitors of effector cells that was similar to that of young mice. Both infant and old mice had plastic-adherent suppressor cells in their spleens, which could strongly inhibit NK activity. In addition, both infant and old mouse spleen cells contained nonadherent suppressor cells, which had a higher density on Percoll gradients than NK cells. Thus, several factors appear to contribute to the age-related regulation of NK activity in mice.
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PMID:Studies on the mechanism of low natural killer cell activity in infant and aged mice. 294 43

The effect of dietary tyrosine and phenylalanine restriction on splenic natural killer (NK) cell activity was studied in tumor-free B6D2F1 and NIH nude mice and in B16 bladder-6 (BL6) melanoma-bearing B6D2F1 mice. This dietary restriction was found to suppress the naturally elevated NK-cell activity of nude mice and to induce a specific lymphocytopenia in B6D2F1 mice fed the restricted diet for a prolonged period. Baseline NK-cell activity was significantly lower in tumor-free B6D2F1 mice fed a diet restricted in tyrosine and phenylalanine (restricted diet) than in tumor-free mice fed a basal diet. Similar kinetics of activation after a single i.p. injection of 100 micrograms of polyinosinic:polycytidylic acid (poly I:C) were observed in mice fed both diets. NK-cell activity was not significantly augmented after i.v. inoculation of BL6 melanoma, irrespective of the diet fed; however, it was enhanced in tumor-bearing mice after poly I:C injection. This augmentation was similar to that observed in tumor-free mice. Spleen cells from mice fed either diet were responsive to stimulation of NK-cell activity after in vitro incubation with interleukin-2. These results indicate that dietary restriction of tyrosine and phenylalanine, a potentially useful therapeutic adjunct known to lower NK-cell activity, does not significantly interfere with poly I:C or interleukin-2 induction of NK cells. Our results also demonstrate that, while this dietary restriction causes lymphocytopenia, no effect of the diet could be found on total serum IgG or circulating immune complex levels.
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PMID:Response of natural killer cells from dietary tyrosine- and phenylalanine-restricted mice to biological response modifiers. 296 70

Supernatants from cultures of mouse and human tumour cells inhibited the production of interleukin-2 (IL-2) by stimulated mouse spleen cells. The tumour cells tested, all of which were active, included a mouse and a human melanoma, three methylcholanthrene-induced fibrosarcomas of mice, and human HeLa cells. Supernatants from normal mouse and human fibroblasts were inactive. Inhibition was dose-dependent. Spleen cells from aged mice were more susceptible to inhibition than spleen cells from young mice. When tumour cell culture supernatants were fractionated on Sephacryl S-300, two peaks of activity were found, with apparent molecular weights of approximately 50 and 18 kD. Supernatants from tumour cell and fibroblast cultures caused variable, but generally weak, inhibition of responses of lymphoblasts to IL-2. It is suggested that inhibition of IL-2 production may be an important mode of action of tumour cell products that inhibit cell-mediated immunity.
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PMID:Inhibition of cell-mediated immunity by tumour cell products: depression of interleukin-2 production and responses to interleukin-2 by mouse spleen cells. 297 6

Mice were infected intravenously with 1.0 mg of Mycobacterium bovis BCG. At various times thereafter, spleen and peripheral lymph node cells were stimulated with concanavalin A for 18 to 20 h, and their capacity to produce interleukin-2 (IL-2) was evaluated by means of a T-cell blast proliferation technique. A depression of IL-2 production that was complete in the spleen but partial in lymph node cell cultures occurred at 2 to 3 weeks and persisted till weeks 8 to 10 after infection. No direct evidence was found for an active suppressor mechanism depressing in vitro the production of IL-2. In spleen cell cultures the suppression of IL-2 production would result from a functional defect of the IL-2-producing T-cell subset, whereas in lymph node cell cultures the depression mainly results from a relative lack of IL-2-producing cells caused by an accumulation of immunoglobulin-positive and "null" cells. Spleen cells from BCG-infected mice maintained their capacity to acquire IL-2 receptors when activated by concanavalin A.
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PMID:Mechanisms underlying the depressed production of interleukin-2 in spleen and lymph node cell cultures of mice infected with Mycobacterium bovis BCG. 308 45

Spleen cells of X5563 tumor-bearing mice were fractionated with Dolichos biflorus lectin (DBA) into DBA+ (agglutinable with DBA) and DBA- (nonagglutinable with DBA) fractions. The DBA- cells showed antitumor activity specific for X5563 cells in vivo when injected into mice together with X5563 cells (Winn assay) or injected i.p. into mice previously inoculated s.c. with X5563 cells (adoptive transfer) with simultaneous administration of interleukin-2. Both DBA+ and DBA- cells have the cell surface phenotype of Lyt-1-2+, but only DBA- cells exhibit antitumor activity in vivo, while DBA+ cells have stronger cytolytic activity against X5563 cells in vitro than DBA- cells. This cell separation method involving the use of DBA is simple and gives reproducible results and high yields of viable cells.
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PMID:Enrichment of antitumor effector cells that are effective in vivo from spleen cells of tumor-bearing mice through the use of Dolichos biflorus lectin. 309 67

Spleen lymphocytes form 5- to 37-month-old C57BL/6J mice were stimulated by concanavalin A (con A) in vitro, and the interleukin-3 (IL-3) expression was assessed by measuring the IL-3 activity in culture supernatants and the cytoplasmic IL-3 mRNA levels. The activity and mRNA level of IL-3 was maximum at 20 hr after culturing in the presence of con A. The IL-3 activity in the culture supernatants and the IL-3 mRNA level in lymphocytes declined 70% to 80% between 5 and 37 months of age. Northern blot analysis revealed no change in the size of IL-3 mRNA between young and old mice. When the expression of IL-3 and interleukin-2 (IL-2) by con A-stimulated lymphocytes was compared, both interleukins showed a similar declined with age.
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PMID:The age-related decline in interleukin-3 expression in mice. 326 6

We examined the effect of rotation-induced stress on (1) growth of lymphosarcoma tumors; (2) interleukin-2 (IL-2) production; (3) T cell subset distribution; and (4) cytotoxic T cell (CTL) function. In addition, we examined the levels of corticosterone and beta-endorphin as possible mediators of stress-induced immune alterations. Rotation stress induced progressive lymphosarcoma growth, while unstressed mice showed tumor regression after 2 weeks of growth. IL-2 production and CTL activity in stressed animals were significantly lower than controls during the first 2 weeks after initiation of stress. Spleen lymphocytes from stressed and control mice bearing the L3T4 antigen (helper/inducer T cell marker) remained unchanged, while in peripheral blood such cells decreased in stressed but not control animals. This latter pattern was also observed in Lyt 2 positive (suppressor/cytotoxic) cells of both spleen and peripheral blood. Corticosterone levels were elevated for an extended period following initiation of stress, while beta-endorphin levels remained similar to those of the controls. Although these data do not directly establish a causal link between immunoinhibition and tumor growth, they clearly demonstrate that stress inhibits a number of cell-mediated immune functions that may be relevant in this regard.
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PMID:Stress-induced decline in immune responsiveness in C3H/HeJ mice: relation to endocrine alterations and tumor growth. 326 57

Spleen cells, obtained 2-5 days after in vivo priming with sheep erythrocytes (SRBC), were cultured to determine the presence of plaque-forming cell (PFC) precursors capable of developing into mature PFC under the influence of various stimulants. Lipopolysaccharide (LPS), added together with SRBC at the initiation of a 48-hr in vitro culture, enhanced the PFC response of primed spleen cells. In vivo priming for a minimum of 3 days was required, and maximal numbers of PFC were obtained from spleen cells primed for 4 days. Depletion of T lymphocytes from Day 3-primed spleen cells abrogated LPS-mediated enhancement, and addition of concanavalin A supernatants to the T-cell depleted system restored the enhancement, suggesting that LPS action required co-operation with a product(s) of activated T cells. Addition of various interleukin-2 preparations including recombinant human IL-2 to the system restored the LPS-mediated enhancement. The response of Day 3 cells from which T cells were eliminated as vigorously as possible was similarly restored by the addition of IL-2, LPS and antigen, suggesting that IL-2 reacts directly with PFC precursors that have developed IL-2 receptors. LPS-mediated enhancement, in the presence or absence of T cells, was also markedly dependent on the presence of SRBC during in vitro culture. These data suggest that, in co-operation with IL-2 and other co-factors, antigen plays a significant role in driving the later stages of differentiation and/or division of PFC precursors to mature PFC.
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PMID:Roles of IL-2 and antigen in the later stages of the primary antibody response. 331 78

Spleen cells from BALB/c mice infected with 2 X 10(7) L. major promastigotes and developing progressive disease produced significantly lower levels of interleukin-2 (IL-2) in response to concanavalin A stimulation than did spleen cells from uninfected mice. In contrast, spleen cells from sublethally irradiated and infected mice, which were able to contain lesion development, produced significantly higher levels of IL-2. The increase in IL-2 production closely paralleled lesion regression. Mice protectively immunized by four intravenous injections with lethally irradiated promastigotes also produced enhanced levels of IL-2, which were sustained after challenge infection. In contrast, spleen cells from BALB/c mice given four s.c. injections of irradiated promastigotes produced high levels of IL-2 before but not after infection. These mice eventually produced levels of IL-2 indistinguishable from those of unimmunized mice with progressive disease. There is thus an inverse relation between disease progression and the ability of spleen cells to produce IL-2. Spleen cells from mice with uncontrolled disease not only produced lower levels of IL-2 but also impaired IL-2 production by normal spleen cells. The ability to inhibit IL-2 was abrogated by passing the cells through a Sephadex G-10 column, removal of plastic adherent cells, and removal of carbonyl iron-ingesting cells. Furthermore, Sephadex G-10 column-treated and plastic adherent, nonspecific esterase-positive spleen cells from mice with progressive disease were able to suppress IL-2 production by normal splenic T cells. The suppressive activity of the adherent cells was not affected by treatment with anti-Thy-1.2 antibody and complement. In contrast, adherent spleen cells from uninfected mice were devoid of such suppressor activity. The depressed IL-2 production by spleen cells from progressively infected mice could be restored to that of normal spleen cells by the addition of indomethacin to the culture. There was however, no correlation between IL-2 production and IL-1 activity in infected or immunized BALB/c mice. Thus, it appears that the suppression of IL-2 production is mediated by prostaglandins elaborated by macrophages from chronically infected mice.
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PMID:Suppression of interleukin-2 production by macrophages in genetically susceptible mice infected with Leishmania major. 349 Apr 40

The relationship between the production of interleukin-1 (IL-1) and interleukin-2 (IL-2) after stimulation of human mononuclear cells within an antigenic extract from Candida albicans was analyzed in both responder and nonresponder donors. Culture supernatants from responders contained both IL-1 and IL-2 activity, whereas the supernatants from nonresponders contained only IL-1 and no appreciable IL-2. However, the addition of exogenous IL-2 to nonresponder cultures restored the normal proliferative response. Similar observations were made when cells from mice infected intravenously with high doses of Mycobacterium bovis BCG were cultured; these cells showed a marked impairment of the proliferative response to purified protein derivative. Spleen cells from BCG-induced unresponsive mice failed to produce IL-2 despite the fact that normal IL-1 activity was present in the culture. Again, the addition of exogenous IL-2 fully reversed the proliferative unresponsiveness. Thus, the presence of IL-1 does not necessarily induce production of IL-2, and the proliferative unresponsiveness is therefore due to a primary lack of IL-2.
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PMID:Dissociation between interleukin-1 and interleukin-2 production in proliferative response to microbial antigens: restorative effect of exogenous interleukin-2. 389 32


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