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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A male adolescent with common variable immunodeficiency developed type I diabetes approximately 1 year after the initiation of immunoglobulin therapy. Immunologic evaluation revealed decreased numbers of T cells and an intrinsic B cell defect in immunoglobulin production. Lymphocytes from the patient failed to generate normal suppressor activity. There were no insulin or islet cell antibodies present in the patient's serum or in the commercial immunoglobulin preparations he received. The patient's HLA phenotype included HLA-DR3 and 4, placing him genetically at high risk for type I diabetes.
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PMID:Type I diabetes in an adolescent with common variable immunodeficiency. 252 61

The comparative study of the amino acid sequence of gp120 in human immunodeficiency virus (HIV) strains HTLV-III and ARV-2 and the amino end areas of the growth hormone receptors of human skin and the insulin receptors has been carried out, thus making it possible to predict the existence of two compact domains connected with an area of a peptide chain. This area is incapable of the formation of a compact globular structure due to a high content of the remnants of proline. The data obtained as the result of electron microscopic study in combination with image processing have confirmed the predicted three-dimensional structure of gp120. This study has also shown that the amino acid sequence of some regions in the domains of gp120 has a significant degree of homology with similarly located regions of the growth hormone and insulin receptors; in its turn, this amino acid sequence is homologous to the framework regions of the VH domain of immunoglobulin. Antibodies to this VH domain specifically react with recombinant HTLV-III antigen. On the basis of the data obtained in our experiments and from the analysis clinico-immunological information, we have come to the conclusion that AIDS is an autoimmune disease induced by HIV due to the structural homology of gp120 with highly important receptors of human cells.
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PMID:[The molecular bases of the pathogenesis of AIDS]. 255 69

During the last 25 years the concept of a chronic autoimmune process leading to the development of insulin dependent diabetes (IDD) has emerged. The presence of two animal models for IDD, the BB rat and the NOD mouse, has improved our ability to understand the process leading to beta cell destruction. The hallmark of an autoimmune disease is the characteristic pathologic lesion of mononuclear infiltration of the pancreatic islets. Further histologic studies of the diabetic pancreas have identified the type of cells infiltrating the islets and led to the concept of pancreatic beta cells capable of presenting antigen. The initial description of linkage disequilibrium of HLA DR3 and DR4 alleles with IDD has now progressed to the molecular level with the identification of residue 57 of the HLA DQ beta chain as crucial to the genetic predisposition to IDD. Autoantibodies to cytoplasmic antigens (ICA), surface antigens, or a membrane protein of 64 kDa identified by immunoprecipitation, autoantibodies to secreted products such as insulin and proinsulin, and autoantibodies that are cytotoxic to cultured beta cells are islet specific autoantibodies that have been described. Some are probably only markers of immunologic activity; others might participate in the destruction itself. The use of ICA as a screening tool has been successful in identifying individuals prior to the onset of IDD. Widespread cellular immunological defects have been identified both in animal models and in man. In the BB rat, a seeming paradox of severe immunodeficiency occurs in an animal with autoaggressive destruction of beta cells. More subtle defects in immunoregulation have been described in the NOD mouse and in human IDD. The response of IDD in both animal models and in man to immunomodulation and to immunosuppression offers further evidence of an immunologically mediated disease. However, some therapies in the animal models, not typically considered immunologic, such as protein restriction and insulin therapy, have prevented IDD. The possibility of intervening prior to the onset of clinical disease at the level either of the initial process of recognition of the pancreatic beta cell as a target organ or of the effector mechanism is approaching a reality in human IDD.
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PMID:Insulin dependent diabetes mellitus, an autoimmune disorder? 267 79

The health condition of man has changed considerably since life insurance companies have been established. The initial problem of the companies was the fact that many young persons died from tuberculosis. For many decades persons from families with tuberculosis cases or with underweight were not accepted for insurance on their lives. Nevertheless companies observed many deaths causes by this disease. Medical directors and actuaries studied these cases in detail (dates and numbers), even of the deceased. The resulting statistics formed the premium calculation basis for persons with an increased risk. Comparative studies allowed acceptance for more people. Within the last decades when sulfonamides, antibiotics and insulin were discovered and produced the mortality ratio decreased. Nowadays, even persons who suffered from tuberculosis do not present an increased risk anymore. The life expectancy has doubled during the last century. This is why degenerative diseases increased, especially the coronary heart diseases. While thirty years ago the mortality ratio stood at about 500%, improved medical and surgical therapy made prognosis easier and when risk factors can be eliminated the mortality ratio tends to be less than 200%. Since insulin is available, patients with type I-diabetes do not die anymore in coma, the remaining risk is the sclerosis of the vessels. Diabetes with adults increases with overweight, high blood pressure and hyperlipemia. The mortality ratio depends on these risk factors. Morbus Crohn, first described in 1932, seems to increase. Life insurance needs more long-term statistical data. For only some years we are confronted with the immunodeficiency "Aids".(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Change in the panorama of chronic diseases and their insurability by life insurance]. 273 88

The biological basis for autoimmunity and immunoincompetence in the BB rat has yet to be localized. In spite of normal thymic histology, thymocyte subsets and blastogenesis, thymus gland products (thymosins) have yet to be studied. In the present report, thymus gland function was studied by measuring thymosin alpha 1 levels at one time point in the BB rat compared with control rates, and BB rat responses to exogenous thymosin (Thymosin fraction 5) were observed. At five months of age, BB rats had thymosin alpha 1 levels comparable to Lewis and Wistar furth rats. Thymosin fraction 5 increased the ratio of peripheral blood W3/25 positive to OX8 positive cells, but otherwise had no effect on the BB rats' T-cell immunodeficiency, or frequencies of tissue autoantibodies or insulin-dependent diabetes. Although B-lymphocyte counts were normal in BB rats, splenocyte responses to B-lymphocyte mitogens were depressed. However, thymosin fraction 5 improved the BB rat B-lymphocyte blastogenesis to near normal for Mycoplasma neurolyticum. Coupled with our previous work, our results suggest that the immune derangement in the BB rat resides outside the thymus.
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PMID:Thymosin and the spontaneously diabetic BB rat. 297 10

The pathogenesis of diabetes in C57BL/KsJ-db/db mice has been proposed to entail autoimmune mechanisms. We have combined immunodeficiency genes with the db mutation to determine whether beta cell necrosis and establishment of severe diabetes would occur in the absence of normal T and/or B lymphocyte functions. Inbred mice carrying the recessive mutations, severe combined immunodeficiency (scid), X-linked immunodeficiency (xid), nude (nu), and the Y-linked autoimmune accelerator (Yaa), were crossed with strains congenic for the db mutation. The diabetes syndrome was studied in double homozygotes produced in the F2 generation. In another experiment, C57BL/KsJ-db/db males were made T cell function deficient by adolescent thymectomy followed by lethal irradiation and bone marrow reconstitution. None of these manipulations served to prevent the induction of a severe diabetes syndrome in any of the model systems analyzed. Thus, diabetogenesis characterized by massive necrosis of the pancreatic beta cells and atrophy of the pancreatic islets was observed in both the absence of normal T cell function (as assessed by absence of T cell mitogen response) and humoral autoimmunity against beta cell antigens (insulin, retroviral p73). In conclusion, our data indicate that anti-beta cell autoimmunity is not a primary event in the etiopathogenesis of diabetes in the db/db mouse.
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PMID:Effect of immunodeficiency on diabetogenesis in genetically diabetic (db/db) mice. 355 24

The metabolic and immunological effects of cyclosporin given to prevent diabetes in BB rats were examined. Diabetes-prone (BBdp) and normal (BBn) BB rats received either oral cyclosporin (10 mg X kg-1 X day-1 or its vehicle from age 30-150 days. Six of 21 (29%) vehicle-treated rats became glycosuric, with hyperglycemia, weight loss, and unremitting insulin requirements, and showed destruction of islet beta-cells. Five of 24 (21%) cyclosporin-treated rats became glycosuric, but none demonstrated weight loss, all required insulin only intermittently after onset, and all showed persistence of islet beta-cells. Cyclosporin induced hypoinsulinemic glucose intolerance in BBn rats. Cyclosporin inhibited the normal rise with age of peripheral blood lymphocyte cell numbers, identified with monoclonal antibodies. OX19+ (pan-T) and W3/25+ helper T-lymphocytes were affected, and there was an increase in the large W3/13+ OX19- population characteristic of BBdp rats; in addition, this subset appeared in BBn rats. Cyclosporin also caused the appearance and/or increase in both BBdp and BBn rats of W3/25+ OX19- and OX8+ OX19- subsets. Suppressor/cytotoxic (OX8+) T-lymphocytes and Ia+ cells were less affected. The incidence of hyperglycemia and glycosuria was therefore unaltered by cyclosporin, although the diabetic syndrome was milder. BBn rats receiving cyclosporin showed glucose intolerance, suggesting that in BBdp rats, the net effects of immunosuppression on beta-cell destruction may have been counterbalanced by the direct effect on the same cells. The attenuation of diabetes in BBdp rats occurred through further immunosuppression rather than by correction of its preexisting immunodeficiency.
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PMID:Immunological and metabolic concomitants of cyclosporin prevention of diabetes in BB rats. 356 73

A 65-year-old man with insulin-dependent diabetes developed intractable pruritus preceding weight loss and increasing fatiguability. Esophagogastroduodenoscopy revealed infection with Candida, cytomegalovirus, and Cryptosporidium. His T cell helper/suppressor ratio was inverted, and the serum human immunodeficiency virus (HIV) antibody was positive. Results of an extensive evaluation for internal malignancy were negative. Despite optimal care, the patient died 12 weeks after his initial hospitalization. We believe that HIV infection should be added to the list of underlying disorders that may present with pruritus.
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PMID:Pruritus as a presenting sign of acquired immunodeficiency syndrome. 358 90

We undertook clinical, immunologic, and endocrinologic studies of a family in which two brothers and their two maternal uncles had a similar disorder characterized by hypogammaglobulinemia and isolated growth hormone deficiency. Recurrent sinopulmonary infections were a prominent feature in two patients. All patients had short stature and retarded bone age during childhood, and the adults had delayed onset of puberty. The immunodeficiency was characterized by absent specific antibody production in vivo and impaired immunoglobulin production in vitro. Three of the four patients lacked circulating B lymphocytes, even though tonsils were present in those patients. All patients had deficient growth hormone responses to insulin and arginine or levodopa. These patients have an X-linked recessive disorder, but their immunodeficiency differs from the X-linked immune disorders in the World Health Organization classification; their X-linked pattern of growth hormone deficiency, without other endocrine abnormality, is also unique.
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PMID:X-linked hypogammaglobulinemia and isolated growth hormone deficiency. 718 77

Interleukin-1 beta (IL-1 beta) is a polypeptide produced by a variety of cells of hematological, dermal and neural origin. We have investigated the effect of type I diabetes mellitus and insulin treatment on tissue levels of IL-1 beta using streptozotocin (STZ)-treated mouse as an animal model. Diabetes affected IL-1 beta in a tissue specific manner. For example, IL-1 beta levels (as measured by ELISA) were markedly decreased in the liver and spleen of the STZ diabetic mice. In contrast, the levels of this cytokine remained unalatered in other tissues including kidney, testis, hippocampus and pituitary. Insulin treatment restored the diabetes-related decreases in liver and spleen IL-1 beta levels. Overall, the present data suggest that the abnormalities in hepatic and splenic IL-1 beta levels may contribute, at least in part, to the immunodeficiency and increased susceptibility to infection in diabetes mellitus.
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PMID:Insulin-dependent reduction in hepatic and splenic contents of interleukin-1 beta in experimental diabetes. 759 Jun 11


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