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

Studies with inbred jirds chronically infected (greater than 5 months) with Brugia pahangi have demonstrated splenic suppressor cells which modulate in vitro responsiveness to mitogens and parasite antigens. The stimuli which induce suppression were characterized by analysing the effect of activated cells from inbred normal or B. pahangi-infected jirds on the PHA and PWM responsiveness of cultures on normal cells. Regulatory cells were stimulated in vitro with concanavalin A (Con A; 5 micrograms/ml) or an extract of adult B. pahangi (20 micrograms/ml) for 72 hr and irradiated (1500 rads) prior to cocultivation with normal cells. Addition of Con A-activated normal spleen cells to normal cells produced moderate suppression of PHA and enhancement of PWM responsiveness. However, Con A-stimulated spleen cells from infected animals consistently suppressed both the PHA and PWM responsiveness of normal cells by 80-90%. Spleen cells from chronically infected jirds were also induced by B. pahangi antigen to suppress both the PHA and PWM responsiveness of normal lymphocytes. In contrast, spleen cells from animals 3-15 weeks after infection and lymph node cells from all time points were capable of suppressing only PWM responses when stimulated by antigen. Normal spleen cells were not induced by B. pahangi antigens to exhibit immunoregulatory activity. The suppression mediated by antigen-induced spleen cells from chronically infected jirds was partially or totally alleviated by removal of non-specific suppressor cells which are plastic adherent and cyclophosphamide-sensitive, or by removal of antigen-specific suppressor cells which bear receptors for histamine. the results suggest the involvement of regulatory cell circuits in experimental filarial infections.
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PMID:Immunoregulation in experimental filariasis. IV. Induction of non-specific suppression following in vitro exposure of spleen cells from infected jirds to Brugia pahangi antigen. 623 27

Spontaneously hypertensive male and female rats (SHR) were compared with Wistar/Kyoto (W/K) controls at 15 wk and 80 wk of age. Treatment of the young and old hypertensives with thymosin, fraction 5, lowered the blood pressure within 4 wk of the start of treatment. Following 10 wk of injections, the blood pressures of the hypertensive rats remained at a depressed level for about 6 wk. The thymic hormone raised the depressed spontaneous T-cell rosette formation of the aged hypertensive rat and increased the lymph node T-cell response to the mitogens, Con A and PHA. Thymosin administration over a period of 7 wk increased the size of the aged hypertensive thymus. No similar effect was observed in the W/K. Spleen cell production of prostaglandin E (PgE) was markedly higher in the young hypertensive and immune complex deposition was found in the glomeruli and tubules of the aged SHR kidneys. Thymosin lowered the high level of PgE to normal and decreased the immune complex deposition in the kidney. IgG1 levels were considerably depressed in the SHR as compared to the W/K. Following thymosin administration levels of IgG1 increased 2-fold in both rat strains. Plaque-forming cells from the spleens of the untreated SHR were about 3-fold less than those of the age-matched W/K. Following treatment with thymosin the number of plaque-forming cells of both groups demonstrated a substantial further decrease. Spontaneous hypertension in rats is similar, in certain respects to autoimmune-like diseases in humans with a depression in T-cell activity as well as immune complex deposition; both conditions being altered by exposure to a thymic extract.
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PMID:Immune response modulation in the spontaneously hypertensive rat. 634 14

In this report we provide evidence that suggests that MOPC 104E may come under regulation in highly immunosuppressed hosts depleted of T cells. Mice that are adult thymectomized, total body irradiated, and transplanted with bone marrow cells were able to resist the growth of MOPC 104E cells. Spleen cells from such animals had low NK activity and no cytotoxicity against MOPC 104E, and poor response to Con A, PHA, and LPS. The animals were deficient in Lyt-1+ and Lyt-2+ cells. The growth of MOPC 104E cells was measured by using the circulating level of MOPC 104E IgM in vivo in mice treated by different modalities. We observed that inhibition of tumor growth in vivo varied with the treatment of the host. Growth was inhibited in the host in the following order: ATXBM greater than XBM greater than NORMAL greater than ATx mice.
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PMID:Inhibition of growth of MOPC 104E cells in immunosuppressed mice. 638 85

Male (A/Ph and C3H/Cbi/BOM) mice were used in our experiments. The cell-free supernatants of spleen mixed leucocyte cultures and allogeneic brain cortex cells were collected upon short-term incubation and tested in a comparative study. Spleen and brain low molecular factors were fractionated (ultrafiltration and gel column chromatography) and assayed for their activity in mitogen-induced 3H-thymidine incorporation into spleen lymphocytes. The specific release of the allogeneic spleen fraction (ASF-2) has been observed. A non-specific stimulating effect of ASF-2 on PHA- and LPS-activated spleen lymphocytes was shown. In contrast, a non-specific suppressive effect of brain fraction on PHA- and LPS-stimulated lymphocytes was demonstrated. The opposite effects of spleen and brain factors can be connected with their different composition. The lymphocyte cultures were not affected by spleen or brain factor, when cultured without the addition of mitogen. Positive and negative regulation or modulation of triggering events in lymphocyte activation by these factors can be suggested.
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PMID:Effect of low molecular factors released during allogeneic interactions of leucocytes or brain cells on PHA- and LPS-induced DNA synthesis in lymphocytes. 644 24

Specific pathogen-free B6D2 mice infected intravenously with 10(6) or 10(8) viable BCG Pasteur develop an anti-tuberculous immune response resulting in a progressive decline in viable BCG counts for the spleen and lung. Mice infected with 10(8) bacilli did not develop detectable levels of tuberculin hypersensitivity. Spleen cells harvested from both groups of mice at increasing time intervals after infection were T-cell enriched by nylon wool passage and tested for blast transformation following exposure to PHA or PPD. An early peak in tritiated thymidine uptake was observed following PPD exposure of cells from both the 10(6) and 10(8) groups. Cells from the latter group of animals developed a profound suppression to responsiveness to PPD throughout the remainder of the experiment. If the heavily infected mice were exposed to a regimen of 10 mg isoniazid plus 10 mg rifampin per 100 ml of drinking water for 30 days, the viable BCG population present within the lungs and spleen declined to near undetectable levels. This drop was associated with a decline in supressor T-cell activity demonstrated by appropriate cell-mixing experiments in vitro. The blastogenic responses to both PHA and PPD were substantially restored after 30 days of drug treatment. Treatment of the BCG infected mice within the first 7 days of infection prevented the development of the suppressor T-cell population.
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PMID:Effect of chemotherapy on suppressor T cells in BCG-infected mice. 644 3

Specific pathogen-free B6D2 mice were infected intravenously with 10(8) viable BCG, M. habana or M. simiae and the level of tuberculin hypersensitivity to 2.5 micrograms PPD or cytoplasmic protein antigens (CPA) prepared from the other organisms was determined using the footpad swelling test with increasing time after infection. This was correlated with the growth or persistence of mycobacterial populations within the liver. Spleen cells were removed from these infected mice and the level of blast transformation following exposure to PHA, PPD or M. habana or M. simiae CPA was measured in vitro. Early in the mycobacterial infections (day 14) thymidine incorporation by the spleen cells was significantly enchanced followed by a profound depression in incorporation rates as the infection progressed. The mechanism of this depressed response involved the production of suppressor T cells in the spleen. In the case of the M. simiae or M. habana infection, cells capable of mediating suppression were still present even after 12 months of infection. In the BCG infection, suppressor T cells declined with time so that by 4 months incorporation rates were back to normal and suppressor cells were no longer detectable in the spleens of the infected animals.
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PMID:Development of suppressor T cells in mice heavily infected with mycobacteria. 644 70

Normal mice infected intravenously with 10(6) or 10(8) viable M. avium develop persistent infections of the lungs, liver and spleen. The liver and spleen counts remained relatively constant whereas those for the lung slowly increased until eventually some of the animals began to die as a result of the infection. None of the heavily infected mice developed delayed hypersensitivity (DTH) to the M. avium cytoplasmic protein antigen (CPA). Spleen cells harvested at increasing time periods after the M. avium infection were tested for their blastogenic responsiveness to PHA and M. avium CPA. The presence of suppressor T cells within the heavily infected spleens was demonstrated by means of cell-mixing experiments before and after treatment of the anergic spleen cells with anti-Thy-1.2 antiserum and complement. The specificity of the suppressor T cells was measured in terms of their ability to depress responsiveness to sheep erythrocytes and an allograft challenge. Initially, the suppressor T cell population affected all of the T cell-mediated responses but as the infection progressed, so the non-specific host responses tended to return gradually towards normal, whereas the specific M. avium CPA-mediated suppression persisted largely unchanged.
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PMID:The specificity of suppressor T cells induced by chronic Mycobacterium avium infection in mice. 645 15

Splenic T lymphocytes of aged Lewis rats respond to Con A and PHA with diminished 3H-TdR uptake compared with splenic T lymphocytes of young Lewis rats. After immunization with allogeneic tumor cells, uptake of 3H-TdR in mixed lymphocyte-tumor cultures and T cell cytotoxicity against tumor target cells are significantly lower with spleen cells of aged rats compared with those of young rats. The culture of spleen cells of aged rats with Con A results in a diminished conversion of Ia-positive T cells from Ia-negative precursors compared with similar cultures of spleen cells of young rats. Spleen cells of both young and aged rats produce high amounts of IL-2 in response to Con A stimulation. "Old" T cells, however, bind relatively little IL-2, do not utilize it in culture, and do not respond to exogenous IL-2 with enhanced 3H-TdR uptake as do "young" T cells. In allogeneic MLTC, "old" T lymphocytes produce little IL-2 compared with "young" cells, and both "young" and "old" cells respond to exogenous IL-2 with enhanced 3H-TdR uptake and increased cytotoxic activity. The data suggest defects in the synthesis and/or recognition of IL-2 as well as defects in the regulation of Ia antigen expression may be responsible, in part, for the reduced T cell function in aged animals.
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PMID:T lymphocytes of young and aged rats. II. Functional defects and the role of interleukin-2. 645 82

The i.v. injection of high doses (3 mg) of BCG into C3H mice bearing a transplantable 3-methylcholanthrene-induced fibrosarcoma caused the regression of a significant proportion. This effect was most evident when the BCG was injected on the day of the graft, or 7 days later. The injection of this agent either 14 days before the graft, or in low doses (0.1 or 0.5 mg), or directly into the tumour (i.t.) only prolonged the survival of the animals. Spleen cells from systemic high-dose BCG-treated mice were found to exert a strong nonspecific cytostatic effect in vitro that was not an artefact of the test conditions, and was not expressed by cells from low-dose animals. The cytostatic effect was shown to be caused by cells with the characteristics of macrophages, i.e. they were strongly adherent, unaffected by treatment with anti-Thy 1.2 + C', radioresistant but heat-sensitive, and were detected in BCG-treated "B" mice. The spleens of high-dose BCG-treated mice also contained suppressor cells that were capable of inhibiting the in vitro reactivity of normal T cells to PHA. Like the cytostatic effect, this suppressor activity was not detected in low-dose mice, and the cells responsible had the properties of macrophages; the effect was lost after the removal of adherent cells by sequential exposure to plastic and colloidal iron, but was conserved after treatment with anti-Thy 1.2 + C'. T-cell-deprived animals, such as "B" or nude mice, also developed suppressor-cell activity when treated with systemic high-dose BCG. Close parallels became evident between the in vivo anti-tumour activity of BCG, the in vitro cytostatic effect, and the suppressor-cell activity. We here discuss the possible role of suppressor cells in the mechanism of action of this agent.
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PMID:Possible role of macrophage-like suppressor cells in the anti-tumour activity of BCG. 645 97

Inbred strains of mice inoculated with T. musculi behaved as either sensitive (A/J, CBA/J and C3H/He/J) or relatively resistant (BALB/c, DBA/2, and C57B1/6) with respect to the magnitude of parasitaemia but not to the length of infection. Spleen cells from T. musculi infected C57B1/6 (resistant) and C3H/HeJ (sensitive) mice inhibited the response of normal spleen cells to PHA and ConA; this suppressive activity was concentrated in T-cells and was higher in the resistant mice. However, infection in T-cell-deprived C57B1/6 and C3H/HeJ mice, although more severe and of much longer duration than in the respective control mice, revealed that T-cells were not responsible for the natural resistance to T. musculi.
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PMID:Immunosuppression during Trypanosoma musculi infection in inbred strains of mice. 660 20


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