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)

Complement profiles on 22 hypocomplementemic patients with membranoproliferative glomerulonephritis (MPGN) type I, on 11 with MPGN II, and on 16 with MPGN III, gave evidence that the nephritic factor of the amplification loop (NFa) is responsible for the hypocomplementemia in MPGN II and the nephritic factor of the terminal pathway (NFt) for the hypocomplementemia in MPGN III. In contrast, in MPGN I, there was evidence for three complement-activating modalities, NFa, NFt, and immune complexes. As a result, four different patterns of complement activation were seen. NFa, found in MPGN II, produces a complement profile characterized mainly by C3 depression. In addition, four of seven (57%) severely hypocomplementemic MPGN II patients (C3 less than 30 mg/dL) had slightly depressed levels of factor B, and one of seven (14%) of properdin, but in all the C5 concentration was normal. In contrast, all eight severely hypocomplementemic patients with MPGN II had depressed C5 and properdin levels, and six of eight (75%) depressed levels of C6, C7, and/or C9. Of eight MPGN III patients with moderate hypocomplementemia, 50% had depressed C5 and properdin levels and the remainder, depressed C3 only. This spectrum of profiles is most likely produced by varying concentrations of NFt. In MPGN I, nine of 23 (39%) had a profile indicating only classical pathway activation; seven of 23 (39%), a pattern compatible with NFt alone; four of 23 (9%), evidence for both classical pathway activation and NFt; and three of 23 (13%), a pattern compatible with NFa. The unique multifactorial origin of the hypocomplementemia in MPGN I, often giving evidence of classical pathway activation, together with previously reported differences in glomerular morphology and clinical features at onset, makes it distinct from MPGN III. Depressed C8 levels were found to some extent in all hypocomplementemic states. The levels were uncommonly depressed in patients with NFa, most markedly depressed with NFt, and moderately reduced with classical pathway activation. The cause is not known. Diagnostically, profiles showing classical pathway activation and low levels of C6, C7, and/or C9 are specific for MPGN I. Those showing only classical activation are likewise diagnostic of MPGN I if systemic lupus erythematosus (SLE) and chronic bacteremia are ruled out.
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PMID:Patterns of complement activation in idiopathic membranoproliferative glomerulonephritis, types I, II, and III. 220 97

Intestinal amoebiasis caused by Entamoeba histolytica trophozoites in mice is accompanied by a depression in the ability of this host to develop an immune response to sheep red blood cells. The number of splenic plaque-forming cells was reduced in mice inoculated intracecally with 2.5 x 10(5) trophozoites at 15, 25, 40, 65 and 75 days after infection when compared with non-infected mice. It was found that there was no significant difference between the spleen weight of the infected and non-infected control animals at 5 and 10 days following infection. However, a significant increase in spleen weight was observed by 15 days of infection and the spleens remained enlarged until termination of the experiment at 75 days. Thus, there was an inverse correlation between the PFC response and the spleen weight of infected animals.
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PMID:Immunosuppression and splenomegaly in Entamoeba histolytica infection in mice. 290 86

The effect of benzo(a)pyrene (BaP) at different molar (M) concentrations on the in vitro anti-sheep red blood cell (SRBC) plaque (antibody) forming cell (PFC) response and the one-way mixed lymphocyte response (MLR) was tested. Inhibition of the PFC response and the MLR occurred when spleen cells were exposed to a wide range of BaP concentrations from 10(-4) M to 10(-8) M. Maximum depression of the responses occurred at 10(-5) M for PFC production (47% of controls) and for the MLR (19% of controls) as measured by a stimulation index. No significant loss in cell viability was observed at this or lower molar concentrations of BaP. The non-carcinogenic analog of BaP, benzo(e)pyrene, did not suppress PFC responses at comparable concentrations. This in vitro system will facilitate manipulations of T and B lymphocytes and macrophages (adherent cells) in a controlled culture environment for precisely characterizing the sensitivity of these cells and their subpopulations on exposure to BaP.
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PMID:Suppression of humoral and cell-mediated immune responses in vitro by benzo(a)pyrene. 294 86

A tissue-culture system to stimulate human peripheral blood mononuclear cells (PBMC) has been employed in which IgM plaque-forming cell (IgM PFC) generation in response to sheep erythrocytes (SRBC) is dependent on macrophages and T suppressor and helper lymphocytes. In this system PBMC from normal subjects give IgM PFC responses ranging from 26 to 938 PFC/culture. Heat-aggregated human IgG or immune complexes present for the duration of culture induce a significant depression of PFC. Unaggregated IgG has no effect on the response or only a moderate stimulatory effect at the highest dose. The results of these experiments are compatible with previous results in a murine system, which indicated that Fc gamma receptor-positive (Fc gamma R+) cells in the suppressor subset are the target for aggregated IgG and induce depression of the PFC response. A similar mechanism may be operating in the human system described here, although the target cell has not been identified. These results may reflect a mechanism of immunomodulation dependent on interaction of Fc receptor (FcR) ligands with FcR, which may play a role in the pathogenesis of immune complex disorders.
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PMID:Depression by Fc gamma receptor ligands of SRBC-induced IgM-PFC generation in human blood mononuclear cell cultures. 297 32

Rabbits fed trinitrophenylated bovine serum albumin (TNP-BSA) generated fewer anti-TNP plaque-forming cells but greater numbers of hapten (TNP)-augmentable IgM and IgG PFC following immunization with TNP-Ficoll or TNP-Brucella abortus than did animals not previously fed antigen. Spleen and mesenteric and bronchial lymph nodes were similarly affected. In addition more auto-anti-idiotype (Id) antibody (anti-anti-TNP) was eluted by hapten from spleen cells of antigen-fed rabbits than from spleen cells of control rabbits not prefed antigen. Gel filtration studies ruled out the possibility that the Id binding activity in the eluates was due to immune complexes. The isotype of the anti-Id was IgG except in one rabbit where it was IgM. The results are consistent with the interpretation that the production of auto-anti-Id antibody is one of the factors responsible for the specific depression of the IgM and IgG immune responses which follows antigen feeding. In contrast the antigen feeding resulted in priming for an IgA anti-TNP response without detectable hapten-augmentable IgA PFC.
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PMID:Production of auto-anti-idiotypic antibody during the normal immune response. XII. Enhanced auto-anti-idiotypic antibody production as a mechanism for apparent B-cell tolerance in rabbits after feeding antigen. 309 Dec 66

Acute administration of Aroclor-1254 (500 mg/kg) or 3,4,5,3',4',5'-hexabromobiphenyl (HBB) (2-6 mg/kg) IP, profoundly inhibited the plaque forming response to subsequent challenge with sheep erythrocytes in Ah locus positive (C57Bl/6N or B6C3F1N) mice. These studies showed: the immunotoxicity results paralleled enzyme induction results insofar as HBB was approximately 100 times more potent than Aroclor 1254; neither Aroclor nor HBB treatment caused significant induction in the Ah locus negative DBA/2N mice; when B6C3F1 mice were challenged with sheep red blood cells (SRBC) 6 or 16 weeks post Aroclor 1254 treatment, substantial recovery of a PFC response was observed; when these compounds were administered to older (76-week-old) (B6C3F1 mice, severe depression of a PFC response was observed. In contrast to its profound depression of a PFC response, Aroclor-1254 (up to 1250 mg/kg) caused slight increases in lymphocyte proliferation induced by either T or B cell mitogens. A single 500 mg/kg dose of Aroclor-1254 also suppressed the ability of recipient B6C3F1 animals to reject a challenge with either the syngenic fibrosarcoma (PYB6) or the gram negative pathogen (Listeria monocytogenes).
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PMID:Induction of immunotoxicity in mice by polyhalogenated biphenyls. 309 83

Isovolemic exchange perfusion of conscious normal and splenectomized rats to a Hct of +/- 3% with the perfluorocarbon based oxygen transport fluid, Fluosol-DA 20%, is characterized by: 1) a greater than projected depression of fibrinogen and the plasma globulins and 2) a rapid regeneration of these and certain other plasma proteins. Similar responses were observed in a study of PFC resuscitation of hemorrhagic shock in splenectomized dogs in which there was a selective depression of the platelets, the plasma globulins, IgG and fibrinogen. In the rats, the red cells and platelets required 14-21 days to return to control levels while the leukocytes returned to normal in 1-2 days. The globulins and fibrinogen exhibited a transient rebound response at 3 and 12 hours post exchange respectively with total protein levels restored to control levels at 48 hours. In the shock study, the leukocytes, which remained at control levels throughout the shock period and for 1 hour post resuscitation were 2.5x control levels at 24 hours. The platelets which were depressed to 20% of control levels following resuscitation remained depressed through the 24 hour time course of the study. Implicit in these results is the possibility that; A) thrombosis and B) immunosuppression may be caused by some component(s) of the perfusion/resuscitation fluid.
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PMID:Regenerative responses to exchange perfusion. 317 90

The influence of an infection with P. chabaudi adami on the isotypic distribution of the in vivo antibody response to SRBC was investigated. Previous experiments suggested that the IgG1 isotype was poorly represented in the antibody response to plasmodial antigens and in the non-specific B cell response which accompanies an infection with P. chabaudi. The experiments described here indicated that although the magnitude of the total primary or secondary in vivo PFC response to SRBC was relatively unaffected by infection, the SRBC-specific IgG1 PFC response was depressed. Maximum depression of the IgG1 component of the response was observed when the priming dose of SRBC was administered at the same time as or after infection with P. chabaudi organisms. Coincident with the depression in the IgG1 response in infected mice was a corresponding increase in the SRBC-specific IgM response. The IgG1 depression was not a consequence of different kinetics of the generation of an IgG1 response, since at all times measured, the IgG1-PFC response was lower. In addition, the depressed IgG1 responses occurred only during a viable infection and could not be induced by inoculation of large amounts of irradiated erythrocytic stages of the parasite. These data suggest therefore, that there is a selective depression of IgG1 antibodies (but not those of other isotypes) regardless of antigenic specificity as a result of infection of C57BL/6 mice with P. chabaudi adami.
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PMID:Influence of Plasmodium chabaudi adami on the isotypic distribution of the antibody response of mice to sheep erythrocytes. 331 75

Spleen cells from CBA or congenitally athymic ("nude") mice were pretreated with various concentrations of DNP coupled to a copolymer of D-glutamic acid and D-lysine (DNP(37)-D-GL), under various conditions of time and temperature. After washing, they were then cultured for 3 days with the direct B cell immunogen, DNP coupled to Salmonella adelaide flagella (DNP-FLA). Under all circumstances tried, exposure of cells to 1 microg/ml DNP-D-GL caused a 70-100% depression in the subsequent DNP-specific PFC response, and 100 ng/ml caused a lesser but still substantial effect. At the concentrations used, DNP-D-GL did not affect irrelevant antibody responses. Though cells from nude mice responded somewhat less well to DNP-FLA than those from CBA mice, no significant difference in the reaction of the two populations to the tolerogen was noted. This demonstrates that DNP-D-GL can, as previously suspected, directly cause unresponsiveness in B lymphocytes.
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PMID:Induction of B cell tolerance in vitro to 2,4-dinitrophenyl coupled to a copolymer of D-glutamic acid and D-lysine (DNP-D-GL). 457 21

The effects of in vivo C3 depletion on the immune response were examined in rabbits by assaying for splenic PFC after immunizing normal or cobra venom factor-treated animals with aggregated human gamma-globulin. The response to this T-dependent antigen has previously been shown to be regulated such that several cycles of PFC appear following a single intravenous injection of antigen. C3 depletion had no effect on the first peak of PFC (appearing 5 days after injection), but resulted in depression of the second peak of PFC (day 13). In rabbits depleted of C3, antigen localization in splenic germinal centers was markedly decreased. Delaying C3 depletion until after antigen localization had occurred resulted in no depression of the second peak of PFC. These results suggest that one mechanism by which C3 affects immune responses in vivo is via its role in influencing the persistence of antigen. In the absence of C3, no significant localization of antigen occurs, resulting in interference with the cyclical production of antibody.
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PMID:Role of C3 in the regulation of a splenic PFC response in rabbits. 615 91


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