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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera of forty insulin-treated Nigerian diabetics attending the outpatients clinic of the University College Hospital (U.C.H.), Ibadan, and an equal number of non-diabetic control subjects matched for age, sex and social status were tested for presence of complement fixing (CF) antibodies against five viruses: Coxsackie A and B1, mumps rubella and enterovirus group antigen. Antibody levels to Coxsackie B1, mumps, rubella and enterovirus did not show any significant difference between the two groups (P > 0.05). The serum levels of antibody to Coxsackie A virus were significantly higher in non-diabetic controls than in the diabetics (P < 0.05). Previous exposure to these viruses may not be a significant factor in the aetiology of insulin dependent diabetes mellitus in this environment.
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PMID:Complement fixing antibodies against selected viruses in diabetic patients and non-diabetic control subjects in Ibadan, Nigeria. 128 37

Viral infection has been suggested to play a triggering role in the pancreatic beta cell destruction which occurs in insulin-dependent diabetes (IDDM). However, the underlying mechanism of this phenomenon is unknown. In this study a human insulinoma cell line has been infected with measles, mumps and rubella viruses since a temporal association is reported between the clinical onset of IDDM and diseases caused by these viruses. The infection with measles and mumps viruses induced the release of interleukin-1 (IL-1) and interleukin-6 (IL-6) by the cell line as assessed by a bioassay and up-regulated the expression of human leucocyte antigen (HLA) class I and class II antigens as evaluated by cytofluorimetric analysis. Stimulation with rubella virus induced the release of IL-6 only and had no effect on HLA antigen expression. These data show for the first time that IL-1 and IL-6 secretion by an insulinoma cell line may occur after viral infection and suggest that cytokine release and increased expression of HLA molecules by beta cells may act to induce the immune response towards beta cells in IDDM.
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PMID:Viral infection induces cytokine release by beta islet cells. 159 39

In the last few years there is a more frequent appearance of papers which suggest the viral etiology of juvenile diabetes mellitus, where the mumps virus is primarily pointed to as the etiological factor. Since there is a high incidence of diabetes in our Province as well as the presence of an epidemic appearance of mumps infections, we were of the opinion that there was good reason for us to study the influence of mumps infection on glucose tolerance. With our research we have proved that mumps leads to the disturbances of carbohydrate metabolism and this is the case not only in the acute stage of infection but also in the course of a two-year follow-up, and they develop as a consequence of the direct influence of the virus on the beta cells of the pancreas. Glucose tolerance disturbances were not in correlation with the changes on the exocrine part of the pancreas neither in the acute stage nor in reconvalescence. Hereditary factors also didn't influence the more frequent appearance of these disturbances in persons with a hereditary disease, which was confirmed statistically also (X2 = 0.67). By research we have proved that disturbances which take the course of the "slow virus infection" type also occur and that they are statistically more significant (X2 = 22.31) in relation to the glucose tolerance disturbances which develop due to a direct activity of the mumps virus.
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PMID:[Mumps infection and disorders of glucose tolerance]. 180 88

A group of 210 pediatric Type 1 diabetic patients with long duration of illness and their matched controls (age range 2-19 years) were analysed for Coxsackie B4 antibodies in IgG-, IgM- and IgA-antibody classes by enzyme-linked immunosorbent assay (ELISA). About 60% of both patients and controls were seropositive. However, patients had higher prevalence and mean levels of IgA-class antibodies compared to controls. No such difference was found in IgG- or IgM-antibody classes. The elevation of IgA-class antibody levels was evident early after the Coxsackie B4 infection and seemed to persist for several years. IgA-class antibody levels did not differ between sexes in either patients or controls. The elevated levels of IgA-antibodies against Coxsackie B4 virus did not correlate with the elevated IgA antibodies against mumps virus, which served as control antigens. Thus it seems that in IDDM patients the abnormal IgA response against both Coxsackie B4 and mumps virus is antigen-specific.
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PMID:Humoral immunity against viral antigens in type 1 diabetes: altered IgA-class immune response against Coxsackie B4 virus. 242 21

It is now well known that insulin-dependent diabetes is a chronic progressive autoimmune disease. The prolonged prediabetic phase of progressive beta-cell dysfunction is associated with immunological abnormalities. A prediabetic period is suggested by the appearance of islet cell antibodies, anti-insulin antibodies, and anti-insulin receptor antibodies. The existence of activated T lymphocytes and abnormal T cell subsets are also other markers. There is still no concensus about the use of the immunosuppression superimposed upon conventional insulin therapy in early diagnosed IDDM and the follow-up of the relatives of IDDM patients who share the genetic predisposition and serological markers for the risk of future onset of IDDM. Treatment in the prodromal period cannot be justified because a link between the disease and early markers such as ICA has not been established with certainty (Diabetes Research Program NIH, 1983). Many immunopharmacological manipulations were reported to be effective in animal models. However, most of them are not readily applied to human subjects. Moreover, IDDM patients are now believed to be heterogeneous, with a complex genetic background. HLA-DR, and more recently DQ, are closely related to the genetic predisposition to IDDM but those genes are not themselves diabetogenic. The contribution of autoimmunity does not appear to be uniform, and in some cases, the contribution of virus is considered more important. There is a lack of a marker for the future onset of IDDM. ICA and ICSA were found after mumps infection, but the existence of those autoantibodies and even the co-existence of HLA-DR3 do not always indicate the future trend to insulin dependency. More precise markers will be disclosed through the biochemical analysis of the target antigens on pancreatic beta-cell for islet antibodies and effector T cells. Much safer and more effective immunopharmacological treatment will be developed through animal experimentation using rat and mouse models. The recent development and interest in this field will further facilitate the attainment of the goal for the complete prevention of IDDM.
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PMID:Immunological aspects of diabetes mellitus: prospects for pharmacological modification. 251 48

The in vitro production of interferon-alpha was studied in cultures of peripheral blood mononuclear cells from children with insulin-dependent diabetes. Significantly lower levels (p less than 0.01) of interferon (median 64 IU/ml) were found in mumps antigen stimulated cultures of IDDM patients compared to control children (median 256 IU/ml) whereas no differences between groups were found in the amount of interferon induced by Coxsackie B pool antigen or live Sendai virus.
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PMID:Low levels of mumps virus antigen induced interferon-alpha production in insulin-dependent diabetes. 256 52

We have found elevated IgA class mumps and Coxsackie B4 virus antibodies and IgA/IgG antibody ratios in type 1 diabetic patients. However, IgA class herpes simplex (HSV1) virus antibodies showed no difference between patients and controls. To study the possible contribution of genetically polymorphic immunoglobulin markers to the pronounced IgA class reactivity Ig allotypes (Gm, A2m and Km determinants) were compared to virus antibodies in diabetic patients and healthy controls. Ig allotypes were equally distributed in both groups suggesting that the genes coding for these structures are not in close linkage disequilibrium with susceptibility gene(s) for type 1 diabetes. Accordingly, pronounced IgA class immune response in diabetic patients is hardly due to Ig allotype related factors. Patients had elevated IgA class mumps and Coxsackie B4 antibodies and IgA/IgG antibody ratios independently of the Gm phenotype group. In healthy subjects but not in diabetic patients IgA class mumps antibody levels and IgA/IgG mumps antibody ratios significantly correlated with the Gm phenotypes. Such Gm association was not observed in Coxsackie B4 or HSV1 antibodies. These results suggest that though Gm phenotypes have a general effect on mumps specific antibody response, some other factors than Ig allotypes are responsible for the elevated IgA class mumps and Coxsackie B antibody levels and IgA/IgG antibody ratios in type 1 diabetes.
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PMID:Immunoglobulin allotypes and virus antibodies in Finnish type 1 diabetic patients. 285 69

Patients from England, Austria, and Australia with recently diagnosed juvenile-onset insulin-dependent diabetes (type 1) mellitus (IDDM) and matched controls were tested for specific IgM responses to Coxsackie B1-5 viruses. 37 of 122 (30%) patients aged less than 15, but only 15 of 204 (6%) controls, were positive (p less than 0.005). Differences in Coxsackie B virus specific IgM responses between patients and controls were statistically significant for patients in England and Austria (p less than 0.005). Coxsackie B virus specific IgM responses were detected in only 3 of 31 patients aged greater than 16. Virus-specific IgM responses were directed against a single serotype, usually Coxsackie B4 or 5, in 23 of 37 (62.5%) children aged less than 15; 10 of 13 (77%) of children aged less than 7 had monotypic responses. Among families of Austrian patients with IDDM, 8 of 79 (10%) siblings had Coxsackie B virus specific IgM responses, 1 of whom subsequently had IDDM, but none of the 80 parents was positive. In contrast, there was no evidence of recent infection by mumps, rubella, or cytomegalovirus (CMV), since mumps-virus specific IgM was present in only 2 of 100 children with IDDM and 5 of 139 controls; no rubella or CMV specific IgM responses were detected in 60 sera from patients with IDDM.
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PMID:Coxsackie B, mumps, rubella, and cytomegalovirus specific IgM responses in patients with juvenile-onset insulin-dependent diabetes mellitus in Britain, Austria, and Australia. 286 61

Insulin-dependent diabetes mellitus (IDDM) results from the destruction of pancreatic beta cells. Viruses have been suggested as one of the possible causes. The evidence for viruses comes largely from experiments in animals, but several studies in humans also point to viruses as a trigger of this disease in some cases. Encephalomyocarditis (EMC) virus, Mengovirus (2T), and Coxsackie B4 virus infect and destroy pancreatic beta cells when inoculated into mice. This results in hypoinsulinemia and hyperglycemia. The development of EMC virus-induced diabetes is dependent on the genetic background of the host and genetic makeup of the virus. Animals with diabetes for several months show some long-term complications, including glomerulosclerosis, ocular changes, and decreased bone formation and mineralization in addition to acute metabolic changes. EMC virus-induced diabetes can be prevented by a live-attenuated vaccine. The capacity of Coxsackie B4 virus to induce diabetes is also influenced by the genetic background of the host. However, Mengovirus-induced diabetes is not dependent on the genetic background of the host. In contrast to the EMC, Mengo, and Coxsackie B4 viruses, reovirus type 1 seems to be somehow associated with an autoimmune response producing a diabetes-like syndrome in suckling mice. This virus produces an autoimmune polyendocrinopathy that results in very mild and transient glucose intolerance. Several common human viruses including mumps, Coxsackie B3 and B4 viruses, and reovirus type 3 can infect human beta cells in culture and destroy them. A variant of Coxsackie B4 virus has been isolated from the pancreas of a child who died of acute-onset IDDM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Perspectives on the role of viruses in insulin-dependent diabetes. 299 65

Type 1 diabetes mellitus is thought to derive from organ-specific autoimmune reactions, probably triggered by environmental factors. In view of the possible involvement of mumps virus and reoviruses in the pathogenesis of autoimmune endocrine disease, serum antibody levels to these viruses were measured in newly-diagnosed diabetic patients aged 5 to 25 years and in matched control subjects. Diabetic patients showed a significantly lower prevalence and reduced titers of antibodies to mumps and reoviruses. By contrast, the antibody response to measles virus (a non-diabetogenic agent) was remarkably similar in the two groups. It is suggested that individuals with an impaired humoral response to some viral agents are at increased risk of developing diabetes when exposed to pancreotropic viruses.
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PMID:Role of antecedent mumps and reovirus infections on the development of type 1 (insulin-dependent) diabetes. 302 16


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