Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult AKR and C58 mice injected intramuscularly with murine sarcoma virus, Moloney isolate (M-MSV), developed high incidence of nonregressing local tumors. Histologically, these tumors revealed the typical pleomorphism of M-MSV sarcomas; in some cases, however, neoplastic tissue showed a nodular or diffuse growth of monomorphic myoblastlike cells, reminiscent of clonal aggregates. No depression of immune reactivity was found in M-MSV-injected mice as evaluated by direct hemolytic plaque-forming cells against SRBC and by virus-neutralizing antibody production. The MSV recovered from the induced tumors proved to be, by neutralization assay, a Gross (G)-MSV pseudotype. Moreover, tumor cell suspensions absorbed out cytotoxic antibody directed against G-cell surface antigens. Therefore, the conclusion was drawn that MSV with envelope characteristics of endogenous G leukemia virus had formed in vivo through a phenotypic mixing phenomenon. The failure of tumors to regress has been interpreted as mainly due to the partial unresponsiveness of host immune reactivity towards G-MuLV specified antigens. Since MSV-tumors arose in AKR mice after a very long latent period, the possibility was considered that this relative resistance might depend on immunologic mechanisms. In fact, M-MSV-injected AKR mice immunodepressed by goat antimouse lymphocyte serum or rendered partially tolerant by neonatal M-MuLV inoculation developed sarcomas with higher incidence and with a shorter latency. Furthermore, the MSV recovered from these early tumors proved to be the original Moloney pseudotype.
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PMID:Tumor induction by murine sarcoma virus in AKR and C58 mice. Reduction of tumor regression associated with appearance of Gross leukemia virus pseudotypes. 460 45

The essential role of continuous antigenic stimulation in the development and differentiation of antibody-forming cells as defined in the X-Y-Z immune cell maturation scheme was examined in these studies. Mice were primed with sheep erythrocytes (SRBC) in an attempt to induce maximum immune progenitor cell conversion (X --> Y). Subsequently antigen was depleted at 1 or 4 days after priming with isologous specific antibody in order to interrupt further immune cell differentiation (Y --> Z). It was reasoned that this condition would result in depression of the functional antibody-producing cell compartment as measured in the intact mice and subsequently in enhancement of the sensitized (Y cell) compartment as measured in the spleen cell transfer system. These data were also correlated with systematic studies of the hyperplasia of the spleen germinal centers. The effect of passive antibody on the primary response to SRBC was a marked decrease indirect and indirect hemolysin-producing cells (DPFC and IPFC). However, there was a lack of correlation in the degree of antibody-mediated 19S and 7S immune cell suppression during the primary response, the DPFC being much less depressed than the IPFC. As measured in the transfer system there was an enhanced 19S sensitized cell compartment and a depressed 7S sensitized cell compartment in 1 day passively immunized mice. This was true whether or not transfers were performed 1, 2, or 4 wk after priming. Similarly, there was an enhanced 19S-sensitized cell compartment with little or no effect on the 7S-sensitized. cell compartment in 4 day passively immunized mice. These data suggest that progeny of the antigen-stimulated progenitor cells (X cell), as a consequence of lack of further antigenic stimulation, were forced into maturation arrest. These studies further demonstrate that isologous passive antibody suppresses germinal center growth regardless of whether the antibody is infused 1, 2, or 4 days after priming. In terms of formation of sensitized cells, the marked depression of 7S sensitized cell compartment after passive immunization at 24 hr in contrast to the enhancement of the 19S sensitized cell compartment corresponds to the suppressed growth of germinal centers during the primary response. Thus, if the germinal center is, as suggested, the site of proliferative expansion of immunocompetent cells, these data indicate that the germinal center growth is related to the 7S antibody response and in the formation of "7S memory."
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PMID:Requirement for continuous antigenic stimulation in the development and differentiation of antibody-forming cells. The effect of passive antibody on the primary and secondary response. 577 91

(CBA X M523)F1, (A X M523)F1 and M523 lymphocytes grafted into lethally irradiated CBA or A mice temporarily lose their capacity to respond to test antigens (SRBC, Vi-antigen, S. typhi). Immunoresponsiveness of F1 cells is affected to a lesser degree in lethally irradiated M523 mice. Depression of response is absent in the CBA leads to F1 combination, in the syngeneic combination and in CBA mice whch have received transplanted cells from F1 hybrids which do not share the M523 mutation. The number of hemopoietic (CBA X M523)F1 colonies was also reduced in CBA mice. Resistance of CBA mice to lymphoid (CBA X M523)F1 cells develops 18 days after birth. It can be reduced by additional recipient preirradiation or preinoculation with (CBA X M523)F1 spleen cells. The abrogated resistance can be partially restored by CBA spleen cells. The activity of (CBA X M523)F1 lymphocytes passaged through CBA spleen is restored in syngeneic F1 secondary recipients but inhibited again in the CBA secondary recipients. These results are consistent with the suggestion that resistance of lethally irradiated CBA mice to hemopoietic and lymphoid (CBA X M523)F1 cells is mediated by immunologically competent, radioresistant recipient cells rapidly reacting to transplantation antigens coded by the mutant H-2Kka allele. These cells temporarily suppress the functional activity of transplanted cells but do not eliminate them.
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PMID:Genetic resistance of CBA and A mice to transplanted lymphoid and hemopoietic cells of CBA.M523 mutants and their F1 hybrids. 610 75

The CY-enhancing effect on DTH response of mice against SRBC was studied by administering to sensitized animals graded amounts of drug at various times during the immune response. The use of a staggered schedule for CY administration made it clear that this enhancing effect could be augmented even further by lowering the standard 200 mg/kg CY dose. Animals immunized on day 0 with 1 X 10(8) SRBC receiving 50 mg/kg doses on days -1, +1, and +4 showed higher DTH responses on day +7 than those similarly sensitized 1 day after the administration of 200 mg/kg body weight. In addition, we wanted to demonstrate that the TDTH effector cell is sensitive to CY in vivo, because a single 50 mg/kg dose inoculated on day +6 can lower by 50% an already established DTH response. This effect was not due to an effect of CY treatment on bone marrow-derived cells recruited to DTH responses; inhibition of DTH responses were transferred with spleen cells of CY-treated recipients. The action of CY is not dose-dependent; the administration on day +6 of a single dose of 200 mg/kg results in no further depression of the DTH reaction. We conclude that CY affects not only T supp cells, but also cell type(s) involved in the cell-mediated response of mice against SRBC, and that the DTH-enhancing effect of the drug is a blend of its action upon all these cells.
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PMID:Effect of fractional cyclophosphamide dosage on sheep red blood cell-delayed-type hypersensitivity response in mice. 622 61

Mouse spleen cells were treated with concanavalin A (Con A) or aggregated mouse IgG2b for 48 h in culture. When cells thus treated were added to fresh mouse spleen cell cultures immunized with SRBC they depressed the response of B lymphocytes as measured by enumerating plaque forming cells (PFC) on the fourth day of culture. When supernatant from cells cultured with IgG2b was added to immunized cultures this resulted in depression of PFC generation similar to that observed by addition of treated cells. The depression observed was essentially in the same range as that observed by addition of Con A treated cells or their supernatant. These observations extend previous work suggesting that IgG2b-induced PFC depression may result from activation of suppressor T cells with elaboration of soluble suppressor factors. This mechanism of immunomodulation may be important in the pathogenesis of immune complex disorders.
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PMID:Depression of direct plaque-forming cell response in mouse spleen cell cultures by aggregated IgG2b-induced factors. 623 6

Immunological cell functions were evaluated during 24, 48 and 96 h O2 exposure in C57Bl/6 mice. A normobaric O2 exposure resulted in depression of delayed type hypersensitivity (DTH) to oxazolone and Staphylococcus aureus antigens. This effect was proportional to the duration of O2 exposure. The antibody response of splenic cells was more rapidly (24 h O2 exposure) and markedly depressed using a T-dependent antigen (sheep red blood cell, SRBC) than with a T-independent antigen (trinitrophenylated lipopolysaccharide, TNP-LPS). While mitogen-induced proliferative responses of spleen cells to Con A and PHA were inhibited after 72 h of O2 exposure, proliferative responses to LPS were inhibited after 96 h. A dissociated antigen and mitogen responses was observed after a short time of O2 exposure (48 h): the antigen specific responses were impaired with a more pronounced effect on T lymphocytes, whereas the DNA synthesis in response to mitogen remained normal.
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PMID:Characterization of immunological depression in mice exposed to normobaric oxygen. 636 Apr 40

Mice infected with Nematospiroides dubius were incapable of responding normally to i.p. or i.v. challenge with SRBC. The HA and PFC response to SRBC in infected animals was characterized by a severe depression of antibody to SRBC on day 4 and a reduced HA peak titre during the following week. The greatest depression of the response to SRBC was associated with an interval of 14 days between infection and the administration of antigen, suggesting that a particular stage of the parasite contributed significantly to immunodepression during this critical period. It was proposed that a combination of parasite induced damage to the intestine, release of parasite secretory/excretory products and loss of appetite by the host produced trauma during which the host was incapable of responding normally. However, mice given low-level and long-standing infections also showed reduced responses to SRBC, although these animals were not severely depressed. It is possible that this generalized weakening of host immunocompetence is the inevitable consequence of a parasite mechanism which operates more specifically to suppress the expression of homologous immunity at the intestinal level.
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PMID:Nematospiroides dubius: factors affecting the primary response to SRBC in infected mice. 636 45

Sera from 60 gastric cancer patients and 20 patients with benign gastric diseases and 8 healthy controls were tested for inhibitory effects on the humoral response to sheep erythrocytes (SRBC) by the plaque forming cell assay (PFC R.I.) using mouse spleen cells and on the phytohemagglutinin (PHA)-induced blastogenesis of normal mouse spleen cells (PHA S.R.). Gastric cancer patient sera showed a significantly lower PFC R.I. than did sera from benign gastric disease patients and from the healthy controls. However, there was no appreciable interstage difference in the degree of depression. The PHA-induced blastogenesis of normal spleen cells was also decreased in the presence of sera from cancer patients, as compared to that in the presence of sera from benign disease patients and from the healthy controls. The depression progressed with advancing stage of cancer. The PHA S.R. showed significant negative correlations with serum levels of IAP, IS, alpha 1-acid glycoprotein and alpha 1-antitrypsin, but there were no such correlations between PFC R.I. and these glycoproteins in serum. There was also no correlation between the values of the PHA S.R. and the PFC R.I. These results suggest that these two assays may depict immunosuppressive activities operating through entirely different mechanisms.
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PMID:Immunosuppressive activity of sera from gastric cancer patients. 643 Nov 62

The expression of surface markers was analyzed on human peripheral blood lymphocytes after exposure to 12-O-tetradecanoylphorbol-13-acetate (TPA), a tumor promoter which is known to have a mitogenic effect on human T-cells. A significant decrease in the proportion of cells capable of binding to SRBC under different experimental conditions (active (EA), high affinity (EH), total (ET) rosettes) was observed after 20 hr exposure to TPA. After 4 days incubation, the ability to form EH and ET rosettes was recovered, while a significant increase in the proportion of EA and temperature stable (ES) rosettes compared with control cultures was observed. Using monoclonal antibodies directed against different T-lymphocyte subpopulations, a depression in the proportion of cells reacting with OKT3 (pan T) and OKT4 (helper/inducer) antibodies was observed, after both early and late exposure to TPA. On the contrary, the positivity with OKT8 (suppressor/cytotoxic) antibody was not affected at any time of culture. These findings suggest that, in normal blood, TPA can modulate the expression of T-cell receptors, and that T-lymphocytes with helper/inducer phenotype appear to be the target of the TPA-induced membrane changes.
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PMID:Changes in SRBC binding capacity and T-surface antigen expression on human peripheral blood lymphocytes stimulated by 12-O-tetradecanoylphorbol-13-acetate (TPA). 668 31

Cytochalasin B (CB) has been shown to be a potent depressant of the antigen-induced clone expansion and terminal differentiation of mouse B-lymphocytes to antibody-forming cells. This effect could be the result of the microfilament-disrupting effect of CB with subsequent inhibition of antigen-sIg complex redistribution, a series of events which seems to be necessary for B-lymphocyte activation. CB is not very active in depressing capping and will inhibit glucose transport. To further investigate the mechanism of action of cytochalasins, the effect of cytochalasin A (CA) on cap formation and plaque-forming cell generation was studied, since CA is less inhibitory of glucose transport and more inhibitory of cap formation. The results presented here indicate that complexes of anti-Ig-sIg will be prevented from capping by as little as 1 microgram of CA, a quantity sufficient to depress markedly the generation of plaque-forming cells to SRBC in culture. These results further confirm our conclusion that the depression of B-lymphocyte activation may be related to the depression of cap formation. It also strongly suggested that inhibition of glucose transport can be regraded as a negligible factor in this depression.
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PMID:Cytochalasin A inhibits B-lymphocyte capping and activation by antigens. 697 87


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