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)

The Kveim reaction was studied in vivo in 50 patients with sarcoidosis. Commonwealth Serum Laboratories Kveim material and a new Danish Kveim material gave 14 and 8 positive reactions respectively, as well as 6 and 8 equivocal reactions. Forty-six of the patients were also tested in vitro for cell mediated immunity to the Danish Kveim material, using both the leucocyte migration agarose technique and the capillary technique. No significant migration inhibition or stimulation were found. A tuberculin skin test was performed in 49 of the patients, and in 45 a dinitrochlorobenzene sensitivity titer was determined. Both tests revealed a depression of the cell mediated immunity. The serum levels of immunoglobulins IgG, IgA, IgM, IgD, and IgE were determined. The serum of each patient was also examined to determine if organ-non-specific and granulocyte-specific antinuclear factors of IgG class, antibodies against native DNA, rheumatoid factor, mitochondrial antibodies, antibodies against thyroid cytoplasm, and parietal cell antibodies were present. IgG levels were above normal in 28 patients; IgE was above normal in 10 patients, 4 of whom were atopics or had an atopic disposition. Organ-non-specific antinuclear factors were present in 17 patients.
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PMID:Humoral and cellular immunity in sarcoidosis. 64 46

Reaginic antibodies belong to IgE, which represents a distinct immunoglobulin class. Human IgE binds with basophil granulocytes and mast cells through the Fc portion of the molecules and mediates the release of chemical mediators that cause allergic symptoms. The initial step of the reaginic hypersensitivity reaction is probably the bridging of cell-bound IgE antibody by antigen. The reaction appears to initiate enzymatic sequences that lead to the release of chemical mediators. Measurement by radioimmunoassay of IgE and IgG antibodies in ragweed-sensitive hay fever patients has revealed immunologic effects of hyposensitization treatment. Experimental models for the immunotherapy in inbred mice strongly suggest that the major immunological effect would be depression of helper function of antigen-specific T cells. The results suggest logical approaches to improve the effect of the treatment.
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PMID:Immunoglobulin E. Current status and clinical laboratory applications. 77 39

Selected case histories indicate that there is good evidence that atopic disease is associated with severe primary and recurrent ocular herpes. The salient features of the syndrome are that the disease is often bilateral, that recurrences are more frequent, and that the corneal epithelium is often slow to regenerate after disease. Therapeutic difficulties may be encountered because atopic eye disease requires anti-inflammatory therapy which is contraindicated in epithelial herpes. Keratoplasty in herpetic disease in the presence of vascularization or atopic eye disease should be avoided, as an augmented homograft reaction is also an occasional complication. Screening of patients for serum immunoglobulins and cellular immunity using in vitro lymphocyte transformation and macrophage migration inhibition tests, failed to reveal any group evidence of immune deficit, but there was evidence of this in some individuals. The most serious management problems occurred in the presence of raised IgE levels. In a group of patients with keratoconus, IgE was raised in 17 per cent, and there was a depression of IgA in 8 per cent. A knowledge of the serum innumoglobulin levels can be of help in the management of the keratoconus patient in the postoperative period after keratoplasty.
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PMID:Herpes simplex keratitis and keratoconus in the atopic patient. A clinical and immunological study. 77 99

Three cases are described showing a seasonal exacerbation of their nephrotic syndrome in association with an atopic trait and grass pollen allergy. The first patient has a history of four consecutive seasonal relapses each requiring steroid therapy. Following a course of desensitization injections he has now been free of relapse for 3 consecutive years. The second patient has also had a recurrent steroid-sensitive nephrotic syndrome often associated with the pollen season and allergic rhinitis. In this patient a course of cyclophosphamide has reduced his tendency to relapse. The third patient who has been on continuous prednisone therapy shows a seasonal increase in proteinuria. Serum changes in the first two patients include: a seasonal rise in total and grass pollen specific IgE; the continued presence of grass pollen specific IgG throughout the year but with a reduction during the pollen season in association with a more pronounced fall in the total IgG level; a depression in the C3 level in association with each major relapse; a mild rise in the I-K titre and a positive result in the Clq test for circulating complexes. A renal biopsy performed on the first patient when in relapse showed minor histological changes only and IgG, IgM, IgA, IgD, IgE, C3 and fibrinogen were undetectable by immunofluorescent examination. The probable mechanism for the development of proteinuria in these patients is discussed.
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PMID:Seasonal nephrotic syndrome. Description and immunological findings. 80 95

The cycle of events which leads to an impairment of the immune response in the malnourished child includes poverty, food deprivation and frequent infections. It is of great significance, however, that the marked suppression of the immune response can be repaired reasonably promptly, if the disease commences after the child has attained 1 year of age. Prenatal infection not only generates growth retardation but also a higher maternal to foetal IgG ratio, higher IgM in the neonate and a sustained immune depression. Passive cutaneous anaphylaxis measurements in the baboon skin and specific IgE determinations reveal that the elevated IgE in PEM is due to parasitic infestation and common allergens and has little or no relationship with decreased T-cell function.
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PMID:Malnutrition and impaired immune response to infection. 82 83

The effect of components P530 and P29, isolated from Ascaris suum adult worm extract (ASC), on the heterologous IgE antibody response was studied in guinea pigs. Groups of 7 guinea pigs were immunized ip with 50 micrograms of ovalbumin (OA) alone or mixed with 200 micrograms of each component precipitated in an alum gel. The primary and secondary IgE antibody response was evaluated by passive cutaneous anaphylaxis reaction (PCA). Immunization of guinea pigs with P29 plus ovalbumin (OA) resulted in a significant increase in the level of serum IgE anti-OA antibodies, especially in the secondary response (almost 8-fold higher when compared with control group). This potentiated response was not observed when the animals received OA plus P530 or the crude extract. Indeed, the P530 component, as well as the crude extract, induced a depression of the anti-OA IgE antibody response (2-3 fold decrease when compared with OA-immunized animals). It was also shown that P29, but not P530 or ASC, was capable of eliciting a strong anti-ASC IgE antibody response. These results demonstrate that in guinea pigs these two Ascaris suum components have antagonistic biological effects, one inducing potentiation and the other suppression of the heterologous IgE antibody response.
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PMID:Effect of purified components of Ascaris suum extracts on IgE antibody response in guinea pigs. 134 94

Of 113 methyl isocyanate (MIC)-exposed subjects studied initially at Bhopal, India, 79, 56, 68, and 87 were followed with clinical, lung function, radiographic, and immunologic tests at 3, 6, 12, 18, and 24 months. Though our cohort consisted of subjects at all ages showing a varied severity of initial illness, fewer females and young subjects were seen. Initially all had eye problems, but dominant symptoms were exertional dyspnea, cough, chest pain, sputum, and muscle weakness. A large number showed persistent depression mixed with anxiety, with disturbances of personality parameters. The early radiographic changes were lung edema, overinflation, enlarged heart, pleural scars, and consolidation. The persistent changes seen were interstitial deposits. Lung functions showed mainly restrictive changes with small airway obstruction; there was impairment of oxygen exchange. Oxygen exchange improved at 3-6 months, and spirometry improved at 12 months, only to decline later. The expiratory flow rates pertaining to large and medium airway function improved, but those for small airways remained low. There were changes of alveolitis in bronchoalveolar lavage fluid on fiber optic bronchoscopy, and in 11 cases positive MIC-specific antibodies to IgM, IgG, and IgE were demonstrated. On follow up, only 48% of the subjects were clinically stable, while 50% showed fluctuations. Thirty-two percent of the subjects had lung function fluctuations. Detailed sequential behavior over 2-4 years was predicted for dyspnea, forced vital capacity, maximum expiratory flow rate (0.25-0.75), peak expiratory flow rate, VO2, and depression score. A model for clinical behavior explained a total variance of 52.4% by using the factors of cough, PCO2 and X-ray zones in addition to above five parameters. The behavior of the railway colony group (1640 patients) revealed a similar pattern of illness. When this observed pattern of changes was transferred to the affected Bhopal city sections (with an equitable age-sex distribution), our model results were again validated. Thus the picture of MIC-induced disease seems similar despite the differences for age-sex and initial severity of illness in our cohort and in the population of Bhopal city as predicted by our model.
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PMID:Sequential respiratory, psychologic, and immunologic studies in relation to methyl isocyanate exposure over two years with model development. 139 63

We have determined IgG subclass concentrations in 100 patients with aspirin-induced asthma and 80 healthy controls. Patients on chronic corticotherapy (n = 64) had significantly lower total IgG levels than patients not receiving steroids (n = 36) or controls. Corticotherapy was not associated with changes in the subclass distributions. In patients, the most striking finding was elevation of IgG4. It was not related to corticotherapy or serum IgE levels. The rise in IgG4 was accompanied by a modest, though statistically significant, depression of IgG1. No changes of IgG2 and IgG3 concentrations were observed. Thus, aspirin-induced asthma is characterized by a distinct pattern of distributions of IgG subclasses. It is suggested that in aspirin-induced asthma elevation of IgG4 might result from chronic antigenic stimulation, of viral origin, and that determination of IgG subclass distribution might be of clinical interest.
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PMID:Altered distribution of IgG subclasses in aspirin-induced asthma: high IgG4, low IgG1. 157 20

In Brown-Norway (BN) rats mercuric chloride induces an autoimmune disease characterized by an increase in serum IgE concentration, and by the production of anti-glomerular basement membrane antibodies responsible for a glomerulonephritis with a heavy proteinuria. (i) This disease results from a B-cell polyclonal activation probably due to frequent anti-class II T cells. (ii) The self limitation observed in this model is associated with both a decrease in the frequency of anti-class II T cells and the emergence of CD8+ T cells able to suppress these autoreactive T cells. (iii) In Lewis (LEW) rats which do not develop autoimmunity, HgCl2 provokes the appearance of non-antigen-specific CD8+ T cells responsible for a depression of T-cell functions. The aim of this work was to test the effect of treatment with an anti-CD8 monoclonal antibody (MoAb) in both BN and LEW rats. Anti-CD8 MoAb-treated rats were effectively depleted in CD8+ T cells. However, neither the induction nor regulation phases of mercury-induced autoimmunity were modified in BN rats. Mercury-induced immunosuppression in LEW rats was abrogated; however, depletion in CD8+ T cells did not allow the disease to occur in that strain. Finally, CD8 depletion induced in normal BN rats the appearance of rare anti-class II T cells showing that these cells are normally present in that strain but negatively controlled by suppressor T cells.
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PMID:Role of CD8+ T cells in mercury-induced autoimmunity or immunosuppression in the rat. 213 55

The diagnosis of drug-induced pneumonitis is generally difficult, and it is made clinically by Tamura's criteria. We experienced 12 cases (7 definite and 5 possible cases) of antimicrobial drug-induced pneumonitis (one of case was the first case caused by carbapenem). Symptoms such as fever (11/12), cough (10/12) and dyspnea (10/12) and laboratory data such as eosinophilia (7/12), elevation of IgE (4/6) and hypoxia (11/12) were commonly seen in these patients, although they were not specific. Lymphocyte stimulation test (5/11) and provocation test (4/8) were quite suggestive of drug allergy. Bronchoscopy has been used for confirmation of pneumonitis. Transbronchial lung biopsy revealed alveolitis (4/9) or alveolar fibrosis (3/9), and bronchoalveolar lavage showed lymphocytosis (6/6) and depression of OKT4/T8 ratio (3/5). The combination of bronchoscopic and immunological examinations were more confirmative for diagnosis.
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PMID:Clinical evaluation of 12 cases of antimicrobial drug-induced pneumonitis. 227 3


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