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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mechanisms of depression of contact sensitivity responses in C57BL/10 mice infected with Trypanosoma cruzi were studied. Cellular involvement during sensitization with oxazolone was investigated in mice acutely infected with T. cruzi. Contact sensitivity was not expressed in mice during the latter stages of the acute infection. Spleen cells from sensitized, infected mice which were unable to respond to oxazolone could confer contact sensitivity upon normal syngenic mice as effectively as spleen cells from uninfected, sensitized donors. The ability of mice infected with T. cruzi to respond to an eliciting dose of oxazolone was significantly improved when macrophages from normal syngenic donors were administered to them at the time of skin test. When either normal or infected mice were used as recipients of lymphocytes from sensitized donors, the normal mice responded significantly better than did infected mice after administration of an eliciting dose of oxazolone. An increase in pyroninophilic cells was observed in draining lymph nodes after application of a sensitizing dose of oxaxolone to the ears of either normal or acutely infected mice. These results indicate that suppression of contact sensitivity during acute T. cruzi infection is directed toward the efferent arm rather than the afferent arm of the response.
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PMID:Contact sensitivity responses in mice infected with Trypanosoma cruzi. 10 35

Spleen cells from Trypanosoma congolense-infected mice showed a drastic depression in their capacity to respond to B and T lymphocyte mitogens and to allogeneic spleen cells in mixed lymphocyte cultures. Spleen cells from infected mice were also poor stimulators in mixed lymphocyte cultures. The poor responsiveness or stimulation capacity was not due simply to dilution of relevant B or T lymphocytes by the large number of null cells found in the spleens of infected animals. These null cells expressed approximately eight times more H-2 antigen than spleen cells from normal (uninfected) mice and were devoid of Ia antigens.
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PMID:Immune depression in trypanosome-infected mice. II. Characterization of the spleen cell types involved. 15 19

Specific pathogen-free B6D2 hybrid mice were infected with high (10(8) cells, intravenous), moderate (10(6) cells, intravenous), and low 10(3) cells, aerogenic) doses of viable BCG Pasteur. The growth of the BCG in the lungs and spleens of the three groups was followed over a 90-day period and correlated with the level of tuberculin hypersensitivity. Spleen cells were harvested from the three groups of mice at increasing time intervals and filtered through nylon wool to remove adherent cells, and the level of blast transformation after exposure to phytohemagglutinin and purified protein derivative was determined. Early in the BCG infection both the high- and the intermediate-dose groups showed enhanced thymidine incorporation by the spleen cell cultures, followed by a profound depression late in the infection. At this time, both groups of mice were anergic to purified protein derivative injected into footpads. Cell mixing studies demonstrated the presence of a population of suppressor cells in the spleens of the anergic animals. The suppressive abilities of these cells would be ablated by treatment with anti-Thy-1 antiserum and complement. The aerogenically infected mice were unresponsive to purified protein derivative but showed no evidence of suppressor T-cells. The lack of tuberculin sensitivity in these mice seemed to be due to a lack of sensitized T-cells in the spleen rather than to active immunosuppression.
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PMID:Suppressor T-cells in BCG-infected mice. 15 67

Spleen cells removed from C57Bl/6J mice bearing a methylcholanthrene-induced fibrosarcoma (MC-16) demonstrate suppressed responsiveness of phytohemagglutinin (PHA) and bacterial lipopolysaccharide (LPS) induced mitogenesis as compared to non-tumorous mice. A similar depression of PHA-induced mitogenesis was observed with spleen cells from C3H/HeJ mice bearing syngeneic mammary adenocarcinomas (C3HBA). The administration of indomethacin, a non-competitive irreversible prostaglandin (Pg) synthesis inhibitor, (75 or 100 mug/mouse, IP) on an alternate day basis to groups of tumor-bearing mice of both strains, significantly enhanced immune cell responsiveness to mitogenic stimulation. The addition of indomethacin (10 mug/ml) to cultures of spleen cells from these tumor-bearing mice, as well as to DBA/1J mice bearing the Cloudman S-91 melanoma, enhanced spleen-cell responsiveness to mitogen-induced DNA synthesis by as much as 156%. Indomethacin administration in vivo or in vitro had no significant effect on mitogen-induced DNA synthesis of spleen cells from non-tumor-bearing animals. It is hypothesized that tumors, or tumor-cell antigens, increase Pg production of a population of spleen cells, and that the increased Pg content of the spleen may be important in controlling immune responsiveness in mice.
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PMID:Indomethacin enhancement of spleen-cell responsiveness to mitogen stimulation in tumorous mice. 18 13

Immunosuppressor activity of considerable potency and complexity was generated during the course of chronic, progressive infection of C3H/Anf mice by Mycobacterium lepraemurium. From the 5th through 10th week after inoculation, spleen cells from infected mice mildly but reproducibly suppressed the direct plaque-forming cell response of normal spleen cell cultures to sheep erythrocytes. Suppression at this stage of infection was mediated by cells with macrophage-like characteristics. A marked increase in splenic suppressor activity at 10 to 11 weeks was associated with the appearance of a second suppressor cell subpopulation composed of T lymphocytes. The appearance of these cells was closely related in time to the onset of rapid splenic enlargement and a loss of cutaneous delayed type hypersensitivity to antigens of M. lepraemurium in mice at 10 to 11 weeks of infection. Suppressor cells were not present in peripheral lymph nodes until terminal infection at 22 to 25 weeks. Suppressor spleen cells depressed the T-dependent antibody response most severely, but there was also a direct effect upon B cells as shown by moderate suppression of responses to TNP-LPS and DNP-Ficoll. Spleen cells from 14-week-infected mice generated a soluble suppressor factor(s) that induces depression of moderate severity, however, the immunosuppression by intact cells was far greater.
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PMID:The evolution of immunosuppressive cell populations in experimental mycobacterial infection. 35 Oct 57

Young male crossbred chicks were fed crystalline amino acid diets containing excess L-methionine or DL-homocysteine to evaluate factors causing methionine toxicity. Chicks were fed diets containing graded levels of excess methionine from 0% to 2.0%. Rate of gain was reduced at all levels of excess methionine, but the magnitude of depression was greater between 1% and 2% than between 0% and 1% excess methionine. Methionine accumulated in plasma of birds fed excess methionine, but plasma levels of homocysteine, cystathionine and cystine remained essentially unchanged. Spleen iron levels increased linearly and blood hemoglobin decreased linearly when chicks were fed diets containing greater than 1% excess methionine, a level equivalent to about 3 times the chicks' requirement. Chicks fed 1.36% homocysteine had reduced gain and gain:feed values, but spleen iron and hemoglobin levels were unchanged. 3-Methylthiopropionate, a possible metabolite in a proposed alternate pathway, caused a precipitous increase in spleen iron levels. Various methyl sources (betaine, choline, methyl acetate) when fed in excess failed to increase spleen iron levels. Methyl mercaptan and methyl mercaptoacetate likewise did not result in an increase in spleen iron deposition. Both the hemosiderosis condition and the reduced food utilization caused by excess methionine were reversed by supplemental glycine plus threonine.
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PMID:Factors affecting methionine toxicity and its alleviation in the chick. 66 Feb 99

Spleen cells from mice pretreated with a Trichinella spiralis extract (TsE-mice) showed severe depression of the response to lipopolysaccharide (LPS) and to concanavalin A (Con A), slight depression to phytohemagglutinin (PHA) and normal response to tuberculin purified protein derivative (PPD) as compared to saline-pretreated controls. Mice pretreated with bovine serum albumin (BSA-mice) revealed greatly reduced responses to LPS, somewhat reduced response to Con A, and normal responses to PHA and to PPD. Only TsE-mice showed significant reduction in the number of rosette-forming cells and of direct and indirect plaque-forming cells (DPFC and IPFC). BSA-mice exhibited some reduction of the DPFC only. Direct hemagglutinating (HA) titers were equivalent in the 3 groups after immunization with sheep erythrocytes but facilitated HA titers were depressed in TsE-mice. The total number and the number of viable cells were similar in the spleens of all animals. TsE treatment causes a reduction in the number of T1 lymphocytes and an inhibition of the late differentiation of B cells in the spleen. Suppressor T-cells apparently play a major but not exclusive role in T. spiralis-induced nonspecific immunodepression.
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PMID:Modification of immune competence by parasitic infections. I. Responses to mitogens and antigens in mice treated with Trichinella spiralis extract. 68 66

BALB/c mice infected with Rowson-Parr virus, a lymphatic leukemia virus isolated from the Friend complex, undergo a rapid depression of antibody response. Spleen cells from these mice in culture show a similar deficit in the response to stimulation with sheep red cells and inhibit the reactivity of normal splenocytes. In an attempt to reverse this immunosuppression, near normal responses were obtained in vitro from infected splenocytes by increasing antigen dose, by adding E. coli lipopolysaccharide, or, more effectively, by cocultivating with small numbers of unfractionated or T cell-depleted peritoneal exudate cells (PC), whereas other manipulations proved ineffective. PC did not prevent the inhibition of normal splenocytes by infected spleen cells, but exhibited substantial restorative activity in vivo. In similar experiments, the immunosuppression exerted by the entire Friend complex could be reversed by PC in vitro but not in vivo. These results indicate that a functional deficit of macrophages may be partially responsible for the immunological impairment induced by leukemia viruses and suggest rational approaches to evaluate the relevance of this impairment to oncogenesis.
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PMID:Reversal of immunosuppression induced by murine leukemia viruses. 107 70

This paper reports the determined results of OKT3, OKT4, OKT8, ERFC, smIg and CIC, TMCA, TGA in 31 cases of Graves disease and in 20 normal controls. The results showed that the OKT3, OKT4, OKT8, ERFC were significantly lower than those in the normal controls, whereas the smIg was higher than that in normal controls. The difference between the two groups was very significant. Even though the ratio of OKT4/OKT8 showed no significance of both. Typology of Graves disease according to the theory of TCM, all 31 cases were divided into two types: (1) 14 cases of depression of Liver-energy and asthenia of Spleen; (2) 17 cases of deficiency of yin leads to hyperactivity of Fire. The OKT8 and the ratio of OKT4/OKT8 in the latter respectively were lower and higher than those of the former. The difference between the two types was significant (P less than 0.01, P less than 0.05) whereas the positive rates of the CIC, TMCA, TGA also were higher in the deficiency of Yin leads to hyperactivity of Fire than those in the depression of Liver-energy and asthenia of Spleen. After treatment with combined TCM-WM on 31 cases of Graves disease, it was found that the OKT4, OKT8, ERFC were significantly elevated, the smIg was markedly decreased than those without treatment. It was also found that smIg markedly decreased in two types, OKT8, ratio of OKT4/OKT8 in the latter and ERFC in both types all returned to normal. Remainder indexes had no obvious change before and after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Correlation between syndrome types of traditional Chinese medicine and peripheral T lymphocytes subsets in Graves' disease]. 139 77

Multiple low doses of streptozotocin are known to induce immune-mediated insulin deficient diabetes and depression of immune reactivity. We show here that immune depression by streptozotocin is not general but that some parts of the immune system are stimulated. Spleen cells from streptozotocin-treated mice showed enhanced cytotoxicity against syngeneic islet cells and various tumour cells including insulinoma cells. Several cell types served as effector cells, including macrophages, asialo GM1+ and Lyt-2+ lymphocytes. The increased cytotoxic activity towards islet cells was mostly due to macrophages and to non-asialo GM1+ and non-Lyt-2+ lymphocytes. A higher activation state of macrophages in low dose streptozotocin-treated mice was demonstrated by measurements of superoxide anion release. We conclude that multiple low doses of streptozotocin stimulate 'natural cytotoxicity', i.e. the non-MHC restricted cytotoxic activity of macrophages, T cells and natural killer lymphocytes.
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PMID:Low dose streptozotocin causes stimulation of the immune system and of anti-islet cytotoxicity in mice. 165 63


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