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)

Ataxia-telangiectasia is characterized by endocrine, neurologic, hematologic, hepatic, cutaneous and immunologic abnormalities. The immunologic deficiencies vary considerably from patient to patient, and in each patient with respect to time. The most frequent deficiencies of humoral immunity are diminished or absent serum and salivary IgA, diminished or absent serum IgE and impaired antibody responses to a variety of bacterial and viral antigens. Deficiencies of cellular immunity are commonly found by both in vivo and in vitro analyses. Histologic confirmation of these immunodeficiencies is readily observed in the lymphoid tissue. The thymus, which may be the seat of the primary abnormality in the immunodeficiency syndrome, regularly shows morphologic characteristics of an embryonic thymus.
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PMID:immunodeficiency in ataxia-telangiectasia. 109 83

Congenital deficiencies of developmental hormones, such as growth hormone and thyroxine, are responsible for the thymus-dependent immunodeficiency disease observed in dwarf mice. Such an immunodeficiency state is associated with early aging phenomena. This fact suggests that lymphoid cells and primarily T-derived cells are involved in the control of aging processes.
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PMID:Relation of lymphoid system and hormones to aging. 109 93

Fetal thymus transplantation was performed in three patients with thymic hypoplasia with abnormal immunoglobulin synthesis, one patient with ataxia telangiectasia, and one patient with immunodeficiency with eczema and thrombocytopenia. All patients received transfer factor before transplantation of a fetal thymus i.p. Reconstitution of cell-mediated immunity occurred in three of five patients. Two of the three patients with reconstitution of cell-mediated immunity also had evidence of improved antibody-mediated immunity. Reconstitution of cell-mediated immunity was characterized as occurring rapidly and being of varying duration, and was unassociated with HL-A chimerism. Successful reconstitution of immunity in these patients may have been related to several factors, including the use of fetal thymus less than 6 hr after abortion, i.p. transplantation, and a synergistic effect of transfer factor.
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PMID:Thymus transplantation in patients with thymic hypoplasia and abnormal immunoglobulin synthesis. 120 26

Four infants underwent radical thymectomy for a suspected malignancy of the thymus. Histology revealed no malignant cells. The patients did clinically well as long as 14 years after the operation. There was laboratory evidence for a cellular and humoral immunodeficiency. Affected were mainly the response to oral poliomyelitis vaccinations and the skin tests of delayed type hypersensitivity.
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PMID:Immunological decay in thymectomized infants. 124 40

A retrospective study aiming at detection of heterozygous carriers of blood adenosine deaminase (ADA) deficiency was carried out in nine families known to us because children had died of combined immunodeficiency (SCID). The trait was found in 3 of 9 parent couples, and in 14 other relatives. In two families one homozygous patient was identified. A total of 54 family members and 60 healthy control subjects were tested. Clinically, the patients were all characterized by marked lymphopenia, nearly normal immunoglobulin levels, and inability to produce antibodies. One homozygous patient recovered after transplantation of fetal liver and thymus and is immunologically normal 1.5 years afterwards.
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PMID:Hereditary sever combined immunodeficiency and adenosine deaminase deficiency. 124 64

The expression of regulatory proteins tat, rev, and nef of human immunodeficiency virus type-1 (HIV-1) and tat of HIV-2 was studied in frozen sections of lymph nodes from HIV-1-infected individuals, and various tissues from uninfected persons. In HIV-1-positive lymph nodes, monoclonal antibodies to HIV-1-tat stained solitary cells in the germinal centers and interfollicular zones, and vascular endothelium. Staining by an anti-nef monoclonal antibody was restricted to follicular dendritic cells, whereas anti-rev antibody bound to fibriohistiocytes and high endothelial venules. The antibodies used labeled several cell types in tissues from uninfected individuals. Anti-HIV-1-tat antibodies labeled blood vessels and Hassall's corpuscles in skin and thymus; goblet cells in intestinal tissue and trachea; neural cells in brain and spinal cord; and zymogen-producing cells in pancreas. Anti-rev antibody stained high endothelial venules, Hassall's corpuscles and histiocytes. One anti-nef antibody solely stained follicular dendritic cells in spleen, tonsil, lymph node and Peyer's patches, whereas two other anti-nef antibodies bound to astrocytes, solitary cells in the interfollicular zones of lymph nodes, and skin cells. The current results hamper the immunohistochemical study for pathogenetic and diagnostic use of HIV regulatory protein expression in infected tissue specimens or cells.
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PMID:Epitopes of human immunodeficiency virus regulatory proteins tat, nef, and rev are expressed in normal human tissue. 127 80

The morphology of lymphatic tissues in 43 autopsy cases of children with inherited immunodeficiency states were analysed. Among the more common diseases, such as Di-George-syndrome, CID-patients, congenital agammaglobulinemia Bruton, CVID, selective IG-A deficiency, Wiskott-Aldrich-syndrome, tissue sections of very rare conditions associated with immunodeficiency, e.g. fetopathia diabetica and leprechaunismus, were investigated by routine and immunohistochemical stainings. Clinical history and laboratory data, augmented by the characteristic pathomorphology of lymphatic tissue sections, will establish or at least suggest a definite diagnosis. Since true thymic dysplasia is very rare (or even non-existent) in the human, this term should be abandoned. Severe thymic tissue alterations in SCID-patients, occur secondary to enzyme defects in lymphatic cells. If patients are successfully treated by bone marrow transplantation, the thymus will subsequently develop into a functionally normal organ.
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PMID:[Morphological changes in the lymphatic system of children with hereditary immunologic deficiency syndromes]. 128 43

Catechin derivatives including (-)-epicatechin gallate (ECG), (-)-epigallocatechin gallate (EGCG), (-)-epigallocatechin (EGC) and green tea extract (GTE) were found to inhibit the activities of cloned human immunodeficiency virus type 1 reverse transcriptase (HIV-1 RT), duck hepatitis B virus replication complexes reverse transcriptase (DHBV RCs RT), herpes simplex virus 1 DNA polymerase (HSV-1 DNAP) and cow thymus DNA polymerase alpha (CT DNAP alpha). EGCG and ECG were shown to be very potent inhibitors of HIV-1 RT. According to the IC50 values for HIV-1 RT, these compounds can be ordered as EGCG 0.0066 mumol/L > ECG 0.084 mumol/L > GTE 0.1 microgram/ml > EGC 7.2 mumol/L. DHBV RCs RT was the least sensitive to these compounds. Kinetic study showed that EGCG exerts a mixed inhibition with respect to external template inducer poly (rA).oligo (dT) 12-18 and a noncompetitive inhibition with respect to substrate dTTP for HIV-1 RT. Bovine serum albumin significantly reduced the inhibitory effects of catechin analogues and GTE on HIV-1 RT. In tissue culture GTE inhibited the cytopathic effect of coxsackie B3 virus, but did not inhibit the cytopathic effects of HSV-1, HSV-2, influenza A or influenza B viruses.
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PMID:[The inhibitory effects of catechin derivatives on the activities of human immunodeficiency virus reverse transcriptase and DNA polymerases]. 128 89

Immunotropic activity of artificial beta-carotene was studied in primary immune response to thymus-dependent antigen (sheep erythrocytes) using models of primary (inherent) and acquired (vinblastine-induced) immunodeficiency. The experiments were carried out using two strains of CBA and C57Black mice with dissimilar responses to the antigen. beta-Carotene was found to remove both acquired and inherent immunodeficiency. The immunostimulating effect of the drug studied appears to be related to the activated production of mediators, namely IL-2.
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PMID:[Correction of primary and secondary immunodeficiency with synthetic beta-carotene]. 129 25

The Moloney murine leukemia virus causes thymic leukemias when injected into newborn mice. A major genetic determinant of the thymic disease specificity of the Moloney virus genetically maps to two protein binding sites in the Moloney virus enhancer, the leukemia virus factor b site and the adjacent core site. Point mutations introduced into either of these sites significantly shifts the disease specificity of the Moloney virus from thymic leukemia to erythroleukemia (N. A. Speck, B. Renjifo, E. Golemis, T. Frederickson, J. Hartley, and N. Hopkins, Genes Dev. 4:233-242, 1990). We have purified several polypeptides that bind to the core site in the Moloney virus enhancer. These proteins were purified from calf thymus nuclear extracts by selective pH denaturation, followed by chromatography on heparin-Sepharose, nonspecific double-stranded DNA-cellulose, and core oligonucleotide-coupled affinity columns. We have achieved greater than 13,000-fold purification of the core-binding factors (CBFs), with an overall yield of approximately 19%. Analysis of purified protein fractions by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis reveals more than 10 polypeptides. Each of the polypeptides was recovered from an SDS-polyacrylamide gel, and those in the molecular size range of 19 to 35 kDa were demonstrated to have core-binding activity. The purified CBFs were shown by DNase I footprint analyses to bind the core site in the Moloney virus enhancer specifically, and also to core motifs in the enhancers from a simian immunodeficiency virus, the immunoglobulin mu chain, and T-cell receptor gamma-chain genes.
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PMID:Purification of core-binding factor, a protein that binds the conserved core site in murine leukemia virus enhancers. 130 96


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