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)

Phytohemagglutinin (PHA) is a non-specific stimulant of blastogenic transformation and proliferation of T-lymphocytes in vitro. This material has been used for detection of a reduced lymphoblastic transformation in vitro and, as a skin test, for providing information in the evaluation of cellular immunodeficiency in man (BLAESE et al. 1973). As in sarcoidosis the immunological features are "depression of delayed-type hypersensitivity suggesting T-cell anergy and raised serum immunoglobulins suggesting B-cell overactivity", the authors used PHA skin test in comparison with patients with tuberculosis and M. Hodgkin. PHA positive reactions recorded at 72 hrs. were in 95% for sarcoidosis, 90% for tuberculosis and 5% for M. Hodgkin. But the histological and histochemical investigation of cutaneous biopsies demonstrated three significant differences at 72 hrs. in untreated patients with sarcoidosis compared to the material of tuberculosis patients: formation of lymphatic pseudo-follicles, an increased number of arteriovenous anastomoses and appearance of C-mucopolysaccharide (a histochemical marker of connective tissue in sarcoidosis). There were in sarcoidosis, unlike tuberculosis, blast cells, plasmocytes and a number of lymphocytes at 72 hrs. It is difficult for the authors to explain the different behaviour of the PHA skin test in sarcoidosis and tuberculosis. The appearance of the C-mucopolysaccharide might be a result of the raised serum level of IgM in patients with sarcoidosis.
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PMID:Histological and histochemical pattern of phytohemagglutinin (PHA) skin test in patients with sarcoidosis. 14 70

Two cases of combined immunodeficiency with lymphopenia, thymic dysplasia, and defective immunoglobulin production are reported. Both show selective hypo-gammaglobulinemia (IgG and IgA respectively) and selective hyper-gammaglobulinemia (both IgE, IgA, and IgM respectively). The cases are classified, by correlation of clinical and histopathological data as a variant of Fireman's disease.
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PMID:Combined immune deficiency syndromes with primary T-cell defect and partial B-cell reactive hyperactivity. Immunological and morphological analysis of two unusual cases. 15 Jan 19

The immunopotentiating effect of levamisole was assessed in a double-blind trial in two comparable groups of patients with Down's syndrome, with which the immunodeficiency and susceptibility to infection are known to be associated. One group was given levamisole continuously and at the same dose for 16 weeks, and the other group was given placebo tablets. A checklist was designed to record the type, frequency, and duration of all infections which occurred in the patients, and delayed type hypersensitivity responses to various antigens were measured. There were no differences between the two groups in body weight, number of intercurrent infections, duration of illness, nor was there any change in degree of depression or cutaneous delayed-type hypersensitivity. These findings, taken with claims of success in some patients and failure in others, suggest that levamisole is not a general immunopotentiating agent, although it may have a specific site (or sites) of action on the immune system. If levamisole is to be used more selectively, this action needs to be characterized.
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PMID:Levamisole: lack of immunopotentiation in a controlled trial. 15 Apr 87

The immunologic theory of aging proposes that the normal process of aging in man and all animals is pathogenetically related to faulty immunological processes and may be analogous to a type of autoimmune phenomena ultimately involving all body tissues. It may be said that the sharply increased incidence in elderly humans of the autoimmune and immunodeficiency "diseases of age" are thought to be greatly potentiated by the age-related decline in immune surveillance mechanisms particularly involving self/non-self discriminatory abilities. The major histocompatibility complex has emerged as a complex of "supergenes" coding for antigens whose ultimate biological function may be to serve as recognition units allowing lymphocytes to recognize self from non-self on an immunological basis. Also, recent data are consistent with our supposition that differences in age-specific peaks of various immune functional parameters in genetically homozygous mice may be influenced by genes linked to the major histocompatibility complex. These differences may account, at least in part, for the highly strain-dependent, age-specific incidence of certain diseases, including autoimmune and malignant diseases in the mouse. Heightened susceptibility to develop a particular disease in a susceptible animal occurs when a certain balance is reached between the interplay of immune functional parameters which mature, differentiate, or decline at different rates in the same animal. The age-specificity of this balance may be under partial control of H-2 or HLA-linked genes.
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PMID:Autoimmunity, histocompatibility, and aging. 15 62

A fatal, widespread, polyclonal, B-cell immunoblastic lymphoproliferative disorder developed in three children with combined immunodeficiency shortly after intra-abdominal transplantation of cultured thymus epithelium for immunoreconstitution. All three had surface immunoglobulin-bearing cells (15 to 20 per cent) in the peripheral blood before transplantation and polyclonally elevated immunoglobulins afterward. Abnormal immunoregulation was demonstrated by a lack of concanavalin A-induced suppressor-cell activity in mixed leukocyte culture in all three patients before transplantation and in two afterward. We suggest that the transplant acted as a promoter through immunostimulation or production of promoter factors, and that excessive polyclonal B-cell proliferation resulted because of inadequate immunoregulatory mechanisms. Although this complication occurred in only three of 30 patients with various forms of immunodeficiency treated with cultured thymus, these cases illustrate a potential problem in immunoreconstitution of combined immunodeficiency disorders.
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PMID:Fatal lymphoma after transplantation of cultured thymus in children with combined immunodeficiency disease. 15 33

We have studied three patients with ataxia-telangiectasia (AT) and found two of them to have a normal mixed leucocyte culture stimulating and responding ability. However, all three patients and one parent had defective cell-mediated lympholysis (CML), even in the face of a potent proliferative response to allogeneic leucocytes. None of these patients showed significant proliferative responses to common microbial antigens (tetanus toxoid, Candida albicans, purified protein derivative (PPD), diphtheria toxoid, influenza). Our studies indicate tha the T cell defect in AT preferentially affects certain T cell functions associated with antigen recognition and the generation of allogeneic CML, while sparing the allogeneic proliferative response. The selective deficiency of specific lymphocyte functions in a thymic immunodeficiency with a known defect in DNA repair is consistent with the concept that DNA modulating enzymes are important for T cell function.
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PMID:Selective defects in T cell function in ataxia-telangiectasia. 15 50

We studied a five-year-old girl with several autoimmune disorders and a 16-year-old boy with acquired agammaglobulinemia to determine whether aberrations of immunoregulatory T cells could explain some instances of immunodeficiency or autoimmunity. The normal peripheral blood T-cell population, as defined by specific heteroantiserums, is 20 per cent TH2+ and 80 per cent TH2-. Human suppressor cells are TH2+, whereas helper cells are TH2-. In addition, each subset expresses Ia antigens upon activation. Our patient with autoimmune disease had no demonstrable TH2+ cells, and her lymphocytes could not be induced to suppress. Her circulating T cells were of an activated-helper phenotype, i.e., TH2-,Ia+. In contrast, in the boy with agammaglobulinemia, the T-cell population was predominantly of an activated-suppressor phenotype, i.e., TH2+,Ia+. This patient's T cells abrogated both his own and his histoidentical brother's B-cell secretion of immunoglobulins. We conclude that the characterization of T cells may provide insight into the causes of a number of abnormal immune states in man.
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PMID:Abnormalities of immunoregulatory T cells in disorders of immune function. 15 8

Answers are beginning to emerge to the questions posed in the introduction to the preceding section. In vitro techniques that allow characterization of malignant cells have particular relevance when, as in Hodgkin's disease, the precise identity of the cells remains in doubt. Monolayer tissue cultures derived from Hodgkin's disease tumours and maintained as established cell lines have proven amenable to a variety of cytogenetic, immunological, enzymatic, and ultrastructural studies. Tissue culture experiemnts, in conjunction with meticulous immunological studies of individual Reed-Sternberg cells from non-cultured tumours, suggest that neoplastic cells of Hodgkin's disease are related to, and possibly derived from, cells of the monocyte-macrophage system. The lymphocytes that comprise an integral part of the cellular proliferation and form the basis for histological subclassification of the tumour could be a manifestation of cell-mediated immunity against this non-lymphoid malignant cell. The immunodeficiency of patients with untreated Hodgkin's disease of limited anatomical extent is not the primary event of the disorder and probably not related to the site at which the aetiological agent acts. The deficit does not result solely from impaired T-cell function and appears to arise as a consequence of excessive suppressor cell activity. Inhibitory monocyte-lymphocyte interactions may be one of the causes of defective cell-mediated immunity in Hodgkin's disease. The possible significance of elevated levels of circulating immune complexes in the serum of patients with Hodgkin's disease is indicated by the finding that such complexes react with cells of long-term monolayer tissue cultures derived from the tumour. Circulating immune complexes may be one source for intracellular immunoglobulin in non-cultured Hodgkin's disease cells. The presence of polyclonal immunoglobulin G on the membrane and within the cytoplasm of Reed-Sternberg cells could be due to in vivo binding and ingestion of immune complexes by such cells. The specificity of the interaction between soluble complement-containing immune complexes and neoplastic cells of Hodgkin's disease depends on the nature of the complexed antigen. The complexes could non-specifically attach via an Fc receptor or, if the complexed antigen is identical to a tumour cell antigen, the binding could be specific. If the immune complexes are tumour specific they could provide a source for isolation and identification of tumour-associated antigens. However, the aetiological significance of antigens and putative oncogenic viruses thus far identified in association with Hodgkin's disease remains to be clarified.
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PMID:The immunopathology of Hodgkin's disease. 15 50

An attempt to correct the state of immunodeficiency in old age was made by repeatedly injecting a chemically defined immunostimulating agent, bestatin, to 16 month old (C57Bl/6 x BALB/c) F1 mice. Aged mice were found to have depressed T-cell and B-cell responses but increased ADCC activity. Weekly injections of bestatin over a period of 6 months resulted in varying effects depending on the dose administered. Small doses (10 microgram per injection) were more effective in restoring humoral responses to SRBC rather than delayed-type hypersensitivity reactions, whereas large doses (100 microgram per injection) acted in the opposite way. Macrophage activation was only obtained after the administration of the high doses of bestatin. Continuous treatment with bestatin did not prevent the appearance of suppressor cells induced by ageing. It led to a significant reduction of ADCC activity in aged animals near to the base line value of young animals. Animals were examined for the presence of spontaneous tumours from the end of the treatment until the age of 28 months. A significant reduction of spontaneous tumour incidence was observed in mice given repeated injections of 100 microgram bestatin when compared to untreated aged mice and to mice given the low doses of bestatin.
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PMID:Restoration of impaired immune functions of aged animals by chronic bestatin treatment. 15 63

A case report of a young bull with persistent papillomatosis associated with immunodeficiency is presented. Humoral immune responses were normal but cell mediated immunity was deficient. The possible significance of the findings to pathogenesis and therapy of the disease is discussed.
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PMID:Persistent papillomatosis associated with immunodeficiency. 16 37


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