Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral blood T and non-T lymphoid cells were examined in 31 patients with a variety of primary immmunodeficiencies for their locomotor activity toward casein and endotoxin-activated serum. T cells from 1 and non-T cells from 2 of 7 patients with Bruton type agammaglobulinemia had poor locomotor activity in this system. Both T and non-T lymphoid cells from all patients with common variable immunodeficiency disease had normal locomotor response to casein and EAS. Heterogeneity in locomotor abnormaltiy of T and non-T cells toward casein and endotoxin-activated serum was observed in other immunodeficient patients. No direct correlation was observed between the proportion of cells in the several T cell subsets and the abnormalities of locomotion of T cells.
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PMID:Subpopulations of human T lymphocytes. VIII. Locomotion of lymphocyte subpopulations in patients with primary immunodeficiency disorders. 31 30

Twenty-two patients with general variable immunodeficiency (GVI) and malabsorption syndrome (MS) were followed up for 2-12 years. III degree MS was found in 17 cases. Serum immunoglobulins concentration and T-lymphocyte count were reduced, the latter at the expense of theophylline-resistant and active E-RFC. With casein and milk albumin as the antigens, lymphokine-producing capacity of the mononuclear cells appeared elevated. MS treatment with adjuvant gamma-globulin produced a positive trend in clinical manifestations of the disease, content of T lymphocytes and relevant subpopulations. Long-term results were less favourable: partial compensation with recurrences persisted in 15 patients only. Seven patients died: two of pneumonia, five of cardiac failure and visceral dystrophy. All MS patients are recommended to undergo serum immunoglobulins diagnosis of GVI and in case of its verification to receive life-time gamma-globulin replacement therapy.
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PMID:[General variable immunologic deficiency with malabsorption syndrome]. 239 30

Terminal deoxynucleotidyl transferase (TdT) containing cells were found in the mesenteric lymph nodes of protein deprived and casein re-fed rats. Double immunofluorescence was used to characterize these TdT+ cells according to their surface antigenic phenotype. TdT+ cells expressing T-cell antigen markers recognized by monoclonal antibodies: W3/13 and OX-19 indicated thymic origin. It was found that these cells represented half the existing TdT+ population in the mesenteric lymph nodes. The rest of them presented the Ia antigen which is coded for by the class II major histocompatibility complex and is recognized by the OX-6 mAb. TdT+ cells presenting the OX-6+ phenotype were ascribed to a bone marrow derived subset. These results indicate that, in some instances, i.e., immunodeficiency due to protein deprivation, TdT+ cells may appear in the mesenteric lymph nodes. Their origin may be attributed either to trafficking of immature cells from the thymus or to cells that leave the bone marrow as a consequence of the damage provoked by protein deprivation.
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PMID:Detection of TdT-positive cells in the mesenteric lymph nodes of immunodeficient rats: study of their antigenic phenotype. 248 89

In these studies we describe the production of three mAb raised to an idiotype on an IgG anticasein antibody isolated from the serum of one IgA-deficient blood donor. These are IgM kappa and block the binding of casein Ag to anticasein antibody. Sera of unrelated IgA-deficient donors were tested for the presence of the idiotype; 15 of 56 IgA-deficient sera (25%) contain the anticasein idiotype, whereas 1 of 45 normal sera was positive. Anticasein antibodies as a whole were predominantly of the IgG1 and IgG3 subclass; idiotype-positive anticaseins are predominantly of the IgG1 subclass. For IgA-deficient donors, the relative amount of idiotype-positive anticasein antibody was correlated with the level of anticasein present in the serum. Studies were done to investigate the potential inheritance of the idiotype in families; in three of four families the idiotype was inherited in an apparent autosomal dominant pattern. Our data show that a common cross-reactive idiotype can be detected in the sera of IgA-deficient individuals and their family members. This suggests that V region markers may be conserved in this humoral immunodeficiency disease.
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PMID:Analysis of a common inheritable idiotype in IgA-deficient sera using monoclonal antibodies. 337 94

Lymphocyte and neutrophil locomotion were studied in 23 patients with well defined, primary immunodeficiencies. These included eight patients with common variable immune deficiency, three patients with X-linked agammaglobulinaemia, two patients with the Wiskott-Aldrich syndrome, three patients with ataxia telangiectasia, three patients with immunodeficiency and normal serum immunoglobulin concentrations, one patient with immune deficiency and hyper-IgM syndrome, two patients with Job syndrome and one patient with a granulocyte adherence defect. Random and stimulated lymphocyte and neutrophil migration were evaluated. C5a and casein were used to stimulate lymphocyte migration and C5a and formyl-methionyl-leucyl-phenylalanine (f-MLP) were used to stimulate neutrophil migration. Significantly depressed lymphocyte migration in response to casein and C5a was observed in patients with common variable immune deficiency, patients with immune deficiency and normal immunoglobulin concentration, and patients with Job syndrome. No consistent defect in lymphocyte locomotion was observed in the other patients studied. Neutrophil migration in response to C5a and f-MLP was depressed in Job syndrome, the patient with a granulocyte adherence defect, one of the six patients with common variable immune deficiency and none of the remaining patients. No significant correlation of skin test reactivity and lymphocyte migration was noted, but a correlation between the degree of lymphocyte proliferation in response to phytohaemagglutinin and lymphocyte migration in response to casein was observed. The results presented indicate that aberrations in lymphocyte migration occur in several types of immunodeficiency diseases and that defects in lymphocyte and neutrophil migration can occur simultaneously or totally independent of each other.
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PMID:Abnormalities of lymphocyte locomotion in immunodeficiency disease. 661 60

In casein-induced murine amyloidosis various lines of investigation have implicated immunodeficiency as playing a role in amyloid formation. In this study, the immunopotentiating agent levamisole failed to prevent amyloidogenesis or to accelerate resolution of preformed amyloid deposits in the mouse model. The serum precursor of amyloid, serum amyloid protein A (SAA), was increased by levamisole in both normal and amyloidotic mice.
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PMID:The effect of levamisole in experimental murine amyloidosis. 720 4

This study was performed in 27 HIV-1+ children to characterize the IgA hyperglobulinaemia observed in the serum during the course of HIV-1 infection. By contrast with serum IgG, which increased very early, IgA elevation was related to the decrease of CD4+ cell percentage. It was demonstrated that IgA1 subclass increased selectively. Secretory IgA (SIgA) and IgA and IgG activity to gliadin, bovine serum albumin (BSA) and at a lower level to casein could be detected in the serum at the early stages of HIV infection, but SIgA levels and IgA activity to gliadin further increased during the course of immunodeficiency. By contrast, IgA and IgG activity to tetanus toxoid did not change. These data demonstrate that the hyper IgA, closely related to the degree of immunodeficiency, could be due in part to a disturbance of the gut mucosal immune system. Moreover, impaired intestinal immunity seems to appear very early, and to progress during the course of paediatric HIV-1 infection.
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PMID:Early impairment of gut mucosal immunity in HIV-1-infected children. 791 75

Effects of dietary protein or arginine deficiency on constitutive and lipopolysaccharide (LPS)-induced nitric oxide (NO) synthesis were determined in young rats by quantifying urinary nitrate excretion. In Experiment 1, 30-d-old rats (n = 16) were divided randomly into two groups (n = 8/group) and pair-fed on the basis of body weight semipurified isocaloric diets containing 20 or 5% casein. In Experiment 2, 30-d-old rats (n = 24) were divided randomly into three groups (n = 8) and pair-fed on the basis of body weight purified isonitrogenous and isocaloric diets (composed of amino acids) containing 0.0, 0.3 or 1.0% L-arginine. In both experiments, daily collection of urine was initiated 10 d after the start of pair-feeding. On d 17 after the pair-feeding was initiated, LPS (1 mg/kg body wt) was injected intraperitoneally into rats, and urine was collected daily for an additional 7 d. In Experiments 3 and 4, activities of constitutive and inducible NO synthases were measured in macrophages and various tissues from protein- or arginine-deficient rats (n = 6). Body weight was lower in rats fed the 5% casein diet or the 0.0 and 0.3% arginine diets than in those fed 20% casein or 1% arginine, respectively. Dietary protein or arginine deficiency decreased serum concentrations of arginine and urinary nitrate excretion before and after LPS treatment, indicating impaired constitutive and inducible NO synthesis. Protein malnutrition reduced constitutive and inducible NO synthase activities in brain, heart, jejunum, lung, skeletal muscle and spleen, and inducible NO synthase activity in macrophages. Because NO is a mediator of the immune response and is the endothelium-dependent relaxing factor, impaired NO synthesis may help explain immunodeficiency and cardiovascular dysfunction in protein- or arginine-deficient subjects.
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PMID:Dietary protein or arginine deficiency impairs constitutive and inducible nitric oxide synthesis by young rats. 1039 97

A variety of milk proteins including lactoferrin, angiogenin-1, alpha-lactalbumin, beta-lactoglobulin, lactoperoxidase, casein and the novel whey proteins lactogenin and glycolactin were tested for inhibitory activity toward human immunodeficiency virus-1 reverse transcriptase (HIV-1 RT), alpha-glucosidase, beta-glucosidase and beta-glucuronidase. Lactoferrin exerted the most potent inhibitory action with an IC50 of about 6 microM. Lactoperoxidase, lactogenin, angiogenin-1 and glycolactin inhibited HIV-1 RT activity with decreasing potencies. Beta-lactoglobulin, alpha-lactalbumin and casein displayed little or no inhibitory effect. Succinylation with succinic anhydride augmented the inhibitory effect of glycolactin, beta-lactoglobulin, alpha-lactalbumin, casein and human lactoferrin. The inhibitory effect of the various milk proteins on the activities of alpha-glucosidase, beta-glucosidase and beta-glucuronidase was meager. Succinylation tended to increase the alpha-glucosidase-inhibitory effect of milk proteins but neither their beta-glucosidase-inhibitory nor beta-glucuronidase-inhibitory effect was affected.
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PMID:First demonstration of an inhibitory activity of milk proteins against human immunodeficiency virus-1 reverse transcriptase and the effect of succinylation. 1110 90

The effect of severe protein deficiency at weaning has been studied in bone marrow, which is a primary lymphoid organ. Our experimental model of secondary immunodeficiency in Wistar rats has shown: (1) a decreased number of viable bone marrow cells (P <.0001); (2) diminished percentage of mitosis (P <.01); and (3) severe alteration in the percentage of chromosome pairs 3, 11, and 12 bearing nucleolar organizer regions (NORs) (P <.05). This last finding indicates a poor ribosomal gene activity. These alterations were reverted after the oral administration of a 20% casein diet during 5 to 9 days. However, there were no karyotype variations between the experimental groups. We conclude from these results that severe protein deficiency at weaning alters several aspects of bone marrow cell proliferation and ribosomal gene activity as determined by the number of silver stained nucleolus organizer regions.
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PMID:Cytogenetic studies in bone marrow cells from Wistar rats in protein malnutrition. 1155 33


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