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)

We report four cases of Omenn's syndrome (OS), an autosomal recessive disease characterized by early erythrodermia, protracted diarrhea, severe infections, lymphadenopathy, hepatosplenomegaly, failure to thrive, and leukocytosis with marked eosinophilia. The immunological investigations revealed B lymphopenia with increased levels of serum IgE and marked depression of T-cell activation, not restored by the addition of exogenous interleukin 2 (IL-2). IL-2 and interferon-gamma (IFN-gamma) production in vitro were very low or absent. One patient was treated with HLA-identical bone marrow transplant with a complete remission of the clinical picture and the immunological defect. The infant died of graft versus host disease 4 months after the graft. For the remaining three infants the outcome was also fatal within the first year of life. In conclusion, OS should be considered a severe combined immunodeficiency disease with peculiar clinical, immunological, and histological findings.
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PMID:Clinical and immunological findings in four infants with Omenn's syndrome: a form of severe combined immunodeficiency with phenotypically normal T cells, elevated IgE, and eosinophilia. 311 64

Parasite-specific IgE antibody response was examined in Strongyloides ratti-infected rats. The results showed that the parasite-specific IgE antibody response was generated after a primary infection. However, repeated infections rather depressed the level of parasite-specific IgE antibody in the serum. Immunization limited to specific stages of the parasite revealed that stimulation of parasite-specific IgE antibody was related to the intestinal adult stage. On the other hand, depression of IgE titers was related to the tissue-migrating larval stage. The capacity of the each stage of the parasite to induce specific IgE response may be related to the variable results of the IgE responses in human strongyloidiasis.
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PMID:IgE response in Strongyloides ratti-infected rats with special reference to the life cycle of the parasite. 370 10

Alpha- and gamma-interferon (IFN) production by peripheral blood mononuclear cells (PBMC) from 18 patients affected by primary immunodeficiency syndromes was examined and compared with that of 20 normal donors. Patients included 8 with common variable immunodeficiency (CVI), 2 with congenital agammaglobulinemia, 4 with ataxia-telangiectasia, 2 with hyper-IgE syndrome, 1 with chronic EBV infection, 1 with combined immunodeficiency, and 1 with immunodeficiency with hyper-IgM. No spontaneous IFN production was observed in either patients and controls. Newcastle disease virus-induced alpha-IFN production was found to be normal in all patients. Gamma-IFN was induced by both galactose oxidase and staphylococcal enterotoxin (B). Gamma-interferon production was low or undetectable in patients with ataxia-telangiectasia, in immunodeficiency with hyper-IgM, and in hyper-IgE syndrome. No major defect of gamma-IFN was found in other types of immunodeficiency, despite the presence of occasional low producers (1 of 8 CVI patients and 1 case of congenital agammaglobulinemia). No correlation was found between IFN production and natural killer activity in individual patients. The analysis of lymphocyte subsets by monoclonal antibodies revealed gross imbalances of helper/inducer and suppressor/cytotoxic subpopulations, but no overall correlation could be established with gamma-IFN production. The observation of major defects in gamma-IFN yield only in diseases with depression of T cell-mediated immunity might contribute to a better understanding of the pathogenetical mechanisms in these diseases. Moreover, future studies should monitor these in vitro functions and their modifications by in vitro or in vivo manipulations.
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PMID:Interferon production in primary immunodeficiencies. 609 14

Asthmatic subjects using oral beta-adrenergic agents had significantly lower mean serum IgG levels than asthmatics not taking beta-adrenergic agents (984 vs. 1,195 mg/dl, p less than 0.025). Corticosteroid use had the same effect (920 vs. 1,195 mg/dl, p less than 0.005). Concomitant usage of both agents was associated with further depression of IgG levels. These were no differences between the serum levels of IgA, IgM, IgD, IgE and the complement components C3 and C4 associated with the use of either or both agents. These findings suggest that beta-adrenergic agents, used in pharmacologic doses, may have an effect on the immune system.
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PMID:Effect of beta-adrenergic agents on immunoglobulin G levels of asthmatic subjects. 612 50

The status of suppressor cells in patients with allergic rhinitis or asthma was studied. This latter group showed absent concanavalin A (ConA)-inducible suppressor cell function as measured by proliferative responses to pokeweed mitogen (PWM) and decreased function as measured by responses to phytohemagglutinin (PHA) or ConA. Patients with rhinitis showed values intermediate between normals and asthmatics. Similarly, preincubation in medium enhanced proliferative responses in normal and rhinitis patients but not in asthmatics, suggesting an absence of a short-lived suppressor cell population in the latter group. Suppressor cell function correlated negatively with log10 of serum IgE concentrations. Theophylline-sensitive suppressor cell numbers were slightly decreased in rhinitis patients and significantly so in asthmatics (p less than 0.01). In vitro preincubation of normal lymphocytes with aminophylline or isoproterenol (10 micrograms/ml) enhanced subsequent proliferative responses to PWM. Little enhancement was observed with cells from rhinitis patients, and actual depression was seen with cells from asthmatics, suggesting abnormal immunomodulatory effects of cyclic-AMP active drugs in this group of patients.
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PMID:Suppressor cell function in respiratory allergy. Modulation by aminophylline and isoproterenol. 645 83

A status of suppressor cells in patients with atopic dermatitis was studied. As a group, they showed absent concanavalin A-inducible suppressor cell function as measured by proliferative responses to pokeweed mitogen and decreased function as measured by responses to phytohemagglutinin or concanavalin A. Similarly, preincubation in medium enhanced proliferative responses in normal donors but not in atopic dermatitis patients, suggesting an absence of a short-lived suppressor cell population in the latter group. Suppressor cell function correlated negatively with log10 of serum IgE concentrations. Theophylline-sensitive suppressor cell numbers were significantly decreased in atopic dermatitis patients (p less than 0.01). In vitro preincubation of normal lymphocytes with aminophylline or isoproterenol (10 microgram/ml) enhanced subsequent proliferative responses to pokeweed mitogen. In contrast, actual depression was seen with cells from atopic dermatitis patients, suggesting abnormal immunomodulatory effects of these drugs in the disease.
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PMID:Abnormal suppressor cell function in atopic dermatitis. 645 54

The effect of neonatally initiated injections of anti-mu serum on immunity to reinfection with Schistosoma mansoni in the rat was investigated in vitro and in vivo. Anti-mu treatment resulting in a profound depression of immunoglobulin synthesis dramatically decreased immunity to reinfection assessed by worm recovery technique. Complement-dependent antibody, IgG2a antibody-eosinophil-mediated and IgE-macrophage cytotoxicity reactions were in parallel markedly reduced. These results show the prominent role played by antibody-dependent mechanisms in immunity to schistosomes in the rat.
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PMID:Effect of neonatal injection of anti-mu antibodies on immunity to schistosomes (S. mansoni) in the rat. 676 87

Serum IgE levels were evaluated in 119 untreated and 112 treated patients with Hodgkin's disease (HD). 38 of the nonatopic untreated patients showed significantly increased (> 300 IU/ml) IgE concentrations. No relationship could be found between increased IgE levels and depressed lymphocyte response to phytohemagglutinin (PHA) or the imbalance of TM and TG lymphocyte subsets. On the other hand, the mean level of suppressor activity elicitable from cells of untreated HD patients by concanavalin A preincubation did not differ significantly from that of healthy control subjects. In contrast, in treated patients, where there was a significant reduction in the number of circulating T lymphocytes, a further depression of the lymphocyte response to PHA, a more marked disproportion of TM and TG cell subsets and a noticeable fall in IgE concentration was found. These data suggest that increased IgE concentrations seen in untreated patients with HD are unrelated to the T-cell defects. They also suggest that hyperproduction of IgE is probably not invariably a consequence of a suppressor cell deficiency.
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PMID:Hyperproduction of IgE and T-cell dysfunction in Hodgkin's disease. 696 58

In 30 patients with systemic lupus erythematosus the number of a circulating basophils was countered in different stages of activity. An inverse correlation was found between the absolute basophils count and anti-DNA antibodies and presumptive circulating immune complexes (as judged by polyethylene glycol precipitation of serum). A positive correlation was found between the absolute basophil count and C3 or C4 levels. IgE on the basophil surface was determined by radioimmunoassay in 7 patients. All of them showed a significantly higher surface IgE number. When the count of circulating basophils was roughly normal, 5 out of the 6 patients showed a positive basophil degranulation test with native DNA. These results suggest the existence of an anti-DNA specific IgE in lupus patients. Depression of the circulating basophil count may be a useful index of lupus activity.
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PMID:Evidence of an immediate hypersensitivity mechanism in systemic lupus erythematosus. 696 64

Dialysable transfer factor (TF) was given in 10 paediatric patients with severe atopic dermatitis (AD). Ten patients with AD, matched for age and severity of disease, served as controls. Prior to the therapy with TF and at weekly intervals thereafter, T- and B-cells in the blood, PHA-stimulation, total IgE and specific IgG antibodies to inhalant and food antigens were determined. Therapy with TF was followed by IgE depression in 8/10 patients and was most pronounced in three patients with initially high levels. Some decrease of IgE levels was seen in four controls also, none of them, however, fell to normal levels as was seen in two of the treated patients. Specific IgE levels decreased slightly, but always remained within the pathological range. T-cell counts in the blood increased in 2/10 cases as well as PHA-stimulation, B-cells counts remained within normal limits. Clinical improvement was seen in one patient, five improved slightly and four remained unchanged. Our results indicate, that transfer factor can lower total IgE levels in cases with atopic dermatitis. The effect is most marked in patients with high total IgE levels. Skin involvement, however, does not closely follow in vitro findings.
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PMID:Influence of dialysable transfer factor on IgE concentrations in patients with atopic dermatitis. 697 79


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