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  • 1
    Electronic Resource
    Electronic Resource
    Immunoglobulin Isotype Profile of Tissue Transglutaminase Autoantibodies is Correlated with the Clinical Presentation of Coeliac Disease (2005)
    Oxford, UK; Malden, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 61 (2005), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Coeliac disease (CD) is characterized by the appearance of autoantibodies against tissue transglutaminase (tTG-Ab). Immunoglobulin A (IgA) tTG-Ab have been described as excellent diagnostic markers, but the Ig subclass distribution and the importance of isotype tTG-Ab have not yet been established. In this study, using newly developed isotype- and subclass-specific radioligand assays, we examined anti-tTG IgA1, IgA2, IgG1, IgG4 and IgE antibodies in 30 symptomatic, untreated patients with CD and 22 subjects suspected to suffer from silent CD (sCD). Among 30 patients with CD, 27 (90.0%) were positive for IgA1 tTG-Ab, whereas only 12 (40.0%) had autoantibodies of the IgA2 subclass (P 〈 0.001). IgG1, IgG4 and IgE tTG-Ab were detected in 17 (56.6%), 0 and 3 (10.0%) individuals, respectively. IgA1 was also the predominant anti-tTG subclass in patients with sCD (n = 20, 90.1%), followed by IgA2 antibodies (n = 7, 31.8%), IgG1 antibodies (n = 4, 18.2%), IgG4 antibodies (n = 1, 4.5%) and IgE antibodies (n = 1, 4.5%). The comparison between both groups revealed a significantly higher prevalence of IgG1 antibodies in patients with symptomatic CD (P 〈 0.01). In 10 of 11 subjects undergoing an intestinal biopsy, the diagnosis of an sCD was confirmed. In this subgroup, there was a positive association between the presence of IgA2 and IgG1 tTG-Ab and severe (Marsh 2–3) mucosal abnormalities. In conclusion, patients with symptomatic and sCD predominantly have IgA1 tTG-Ab. IgG1 tTG-Ab are associated with symptomatic disease and, when present in patients with sCD, are correlated with a severe mucosal destruction. These data suggest that tTG-Ab subclasses could reflect inflammatory events associated with epithelial destruction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0300-9475.2005.01549.x
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  • 2
    Electronic Resource
    Electronic Resource
    Combined screening for autoantibodies to IA-2 and antibodies to glutamic acid decarboxylase in first degree relatives of patients with IDDM (1996)
    Springer
    Diabetologia 39 (1996), S. 1351-1356 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin-dependent diabetes mellitus ; antibodies to tyrosine phosphatase IA-2 ; GAD antibodies ; islet cell antibodies ; prediction.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To determine the value of antibodies to the intracytoplasmic domain of the tyrosine phosphatase IA-2 (anti-IA-2 ic) and glutamic acid decarboxylase (GADA) for identification of subjects at risk for insulin-dependent diabetes mellitus (IDDM) we investigated 1238 first degree relatives of patients with IDDM for the presence of anti-IA-2 ic and GADA and compared the results with cytoplasmic islet cell antibodies (ICA). Anti-IA-2 ic were observed in 54 (4.4 %) first degree relatives, in 51 of 86 (59.3 %) ICA positive relatives and in 3 of 4 individuals who developed overt IDDM within a follow-up period of 1 to 28 months. GADA were found in 78 of 1238 (6.3 %) first degree relatives. They were detected in 22 of 35 (62.9 %) sera with ICA alone and in 1 of 3 subjects with anti-IA-2 ic in the absence of ICA. Of the 1238 subjects 37 (3.0 %) sera were positive for all three antibodies. Both anti-IA-2 ic and GADA were positively correlated with high levels of ICA. Anti-IA-2 ic and GADA were detected in 39.1 and 47.8 % of subjects with ICA of less than 20 Juvenile Diabetes Foundation units (JDF-U) but in 66.7 and 76.2 % of individuals with ICA of 20 JDF-U or more, respectively (p 〈 0.05). The levels of ICA and GADA in first degree relatives with at least one additional marker were significantly higher than in subjects with ICA alone (p 〈 0.005) or GADA alone (p 〈 0.03). The combination of anti-IA-2 ic and GADA identified 84.9 % of all ICA positive subjects and 93.7 % of individuals with high level ICA (≥ 20 IDF-U). All 4 individuals who progressed to IDDM had either IA-2 ic or GADA. Our data indicate that primary screening for anti-IA-2 ic and GADA provides a powerful approach with which to identify subjects at risk for IDDM in large-scale population studies which may represent the basis for the design of new intervention strategies. [Diabetologia (1996) 39: 1351–1356]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050582
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  • 3
    Electronic Resource
    Electronic Resource
    Antibodies to the Mr 64,000 (64K) protein in islet cell antibody positive non-diabetic individuals indicate high risk for impaired Beta-cell function (1992)
    Springer
    Diabetologia 35 (1992), S. 550-554 
    Details
    ISSN: 1432-0428
    Keywords: Population study ; 64K antibodies ; islet cell antibodies ; complement-fixing islet cell antibodies ; insulin autoantibodies ; HLA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A prospective study of a normal childhood population identified 44 islet cell antibody positive individuals. These subjects were typed for HLA DR and DQ alleles and investigated for the presence of antibodies to the Mr 64,000 (64K) islet cell antigen, complement-fixing islet cell antibodies and radiobinding insulin autoantibodies to determine their potency in detecting subjects with impaired Beta-cell function. At initial testing 64K antibodies were found in six of 44 islet cell antibody positive subjects (13.6%). The same sera were also positive for complement-fixing islet cell antibodies and five of them had insulin autoantibodies. During the follow-up at 18 months, islet cell antibodies remained detectable in 50% of the subjects studied. In all six cases who were originally positive, 64K antibodies were persistently detectable, whereas complement-fixing islet cell antibodies became negative in two of six and insulin autoantibodies in one of five individuals. HLA DR4 (p 〈 0.005) and absence of asparic acid (Asp) at position 57 of the HLA DQ β chain (p 〈 0.05) were significantly increased in subjects with 64K antibodies compared with control subjects. Of 40 individuals tested in the intravenous glucose tolerance test, three had a first phase insulin response below the first percentile of normal control subjects. Two children developed Type 1 (insulin-dependent) diabetes mellitus after 18 and 26 months, respectively. Each of these subjects was non-Asp homozygous and had persistent islet cell and 64K antibodies. We conclude that 64K antibodies, complement-fixing islet cell antibodies and insulin autoantibodies represent sensitive serological markers in assessing high risk for a progression to Type 1 diabetes in islet cell antibody positive non-diabetic individuals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400483
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  • 4
    Electronic Resource
    Electronic Resource
    Human monoclonal islet specific autoantibodies share features of islet cell and 64 kDa antibodies (1993)
    Springer
    Diabetologia 36 (1993), S. 785-790 
    Details
    ISSN: 1432-0428
    Keywords: Islet cell antibodies ; 64 kDa antibodies ; human monoclonal antibodies ; glutamate decarboxylase ; gangliosides ; Type 1 (insulin-dependent) diabetes mellitus ; islet cell antigens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The first human monoclonal islet cell antibodies of the IgG class (MICA 1-6) obtained from an individual with Type 1 (insulin-dependent) diabetes mellitus were cytoplasmic islet cell antibodies selected by the indirect immunofluorescence test on pancreas sections. Surprisingly, they all recognized the 64 kDa autoantigen glutamate decarboxylase. In this study we investigated which typical features of cytoplasmic islet cell antibodies are represented by these monoclonals. We show by double immunofluorescence testing that MICA 1-6 stain pancreatic beta cells which is in agreement with the beta-cell specific expression of glutamate decarboxylase. In contrast an islet-reactive IgM monoclonal antibody obtained from a pre-diabetic individual stained all islet cells but lacked the tissue specificity of MICA 1-6 and must therefore be considered as a polyreactive IgM-antibody. We further demonstrate that MICA 1-6 revealed typical features of epitope sensitivity to biochemical treatment of the target tissue which has been demonstrated for islet cell antibodies, and which has been used to argue for a lipid rather than a protein nature of target antigens. Our results provide direct evidence that the epitopes recognized by the MICA are destroyed by methanol/chloroform treatment but reveal a high stability to Pronase digestion compared to proinsulin epitopes. Conformational protein epitopes in glutamate decarboxylase therefore show a sensitivity to biochemical treatment of sections such as ganglioside epitopes. MICA 1-6 share typical features of islet cell and 64 kDa antibodies and reveal that glutamate decarboxylase-reactive islet cell antibodies represent a subgroup of islet cell antibodies present in islet cell antibody-positive sera.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00401152
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  • 5
    Electronic Resource
    Electronic Resource
    Immunological heterogeneity in Type I diabetes: presence of distinct autoantibody patterns in patients with acute onset and slowly progressive disease (1998)
    Springer
    Diabetologia 41 (1998), S. 891-897 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Type I diabetes ; slowly progressive Type I diabetes ; autoantibodies ; protein tyrosine phosphatase ; glutamic acid decarboxylase ; islet cell antibodies.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Type I diabetes mellitus may represent a heterogeneous disorder with a distinct pathogenesis in patients with young and adult onset of the disease. To investigate whether serological markers directed to different autoantigens have the potential to distinguish acute onset from slowly progressive Type I diabetes we analysed antibodies to tyrosine phosphatases IA-2/ICA512 (IA-2A) and IA-2β/phogrin (IA2βA), antibodies to GAD65 (GADA) and cytoplasmic islet cell antibodies (ICA) in a non-selected group of diabetic patients clinically classified as having Type I or Type II diabetes at diagnosis. Both IA-2A and IA-2βA were found to be positively associated with onset before the age of 20 years and the presentation of classical features of Type I diabetes. In Type I diabetes 56 % (112/200) of patients were positive for IA-2A and 38 % (76/200) for IA-2βA. In contrast, only 1 of 785 (0.1 %) patients with Type II diabetes had IA-2A and all of them were negative for IA-2βA (p 〈 0.001). Among the patients with Type II diabetes 7.6 % (n = 60) were ICA positive and 2.8 % (n = 22) had GADA suggesting the presence of slowly progressive Type I diabetes. GADA were found in 8 of 60 (13.3 %) ICA positive subjects which was lower than the percentage detected in patients with acute onset of diabetes (115/157 73.2 %) (p 〈 0.001). Blocking of double antibody positive sera showed that only 3 of 8 (37.5 %) patients with slowly progressive diabetes had ICA restricted to GAD or IA-2 whereas ICA were completely inhibited in 12 of 20 (60.0 %) patients with Type I diabetes. Among 193 patients with Type II diabetes available for follow-up, 35 % of ICA positives, 58 % of GADA positives and 60 % of those positive for both markers required insulin by 3 years. However, using strict criteria for the switch to insulin treatment the corresponding sensitivity of each marker was only low (9 %, 10 % and 5 %). We show that clinical subtypes of Type I diabetes are associated with distinct humoral autoimmunity. IA-2A and GADA were associated with classical features of Type I diabetes whereas GADA and an uncharacterized ICA subspecificity indicate slowly progressive disease. [Diabetologia (1998) 41: 891–897]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051004
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  • 6
    Electronic Resource
    Electronic Resource
    Zinc sulphate induces metallothionein in pancreatic islets of mice and protects against diabetes induced by multiple low doses of streptozotocin (2000)
    Springer
    Diabetologia 43 (2000), S. 1020-1030 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Streptozotocin ; metallothionein ; zinc sulphate ; diabetes ; beta cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. Diabetes is induced by multiple low doses of streptozotocin (MLD-STZ) in male mice of susceptible strains. In this model beta-cell injury and T-cell-mediated inflammatory reactions are induced. Probably, reactive oxygen species (ROS) participate in the destruction of beta cells. The effects of ROS can be counterbalanced by several antioxidant systems. One of these is metallothionein (MT), cytosolic proteins that are induced by zinc ions (Zn2+) and scavenge hydroxyl radicals (·OH). The effect of Zn2+ on MLD-STZ-diabetes was studied. Methods. We gave C57BL/6 and (C57BL/6 × SJL)F1 hybrid mice either MLD-STZ or in addition Zn2+-enriched drinking water. We analysed metallothionein ex vivo in pancreatic islets for protein and mRNA concentration for the isoforms 1 and 2. Pancreatic sections were examined by immunohistochemistry for metallothionein and histologically for insulitis. Results. In both strains, Zn2+-enriched drinking water significantly up-regulated metallothionein and prevented MLD-STZ-diabetes and loss of beta-cell function. In the F1 hybrid mice a variant of MLD-STZ-diabetes was observed. These mice developed hyperglycaemia 10 weeks after the first injection of STZ (in contrast to 2 weeks observed in other mouse strains) and pronounced insulitis. The mRNA of the metallothionein isoforms 1 and 2 were constitutively expressed and slightly up-regulated by Zn2+-enriched drinking water. All islets cells stained for metallothionein. Conclusions/interpretations. Drinking water enriched with Zn2+ significantly up-regulated metallothionein production in pancreatic islets of mice and prevented diabetes induced with MLD-STZ. [Diabetologia (2000) 43: 1020–1030]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050009
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  • 7
    Electronic Resource
    Electronic Resource
    No association between islet cell antibodies and coxsackie B, mumps, rubella and cytomegalovirus antibodies in non-diabetic individuals aged 7–19 years (1991)
    Springer
    Diabetologia 34 (1991), S. 835-838 
    Details
    ISSN: 1432-0428
    Keywords: Viral antibodies ; Beta-cell function ; population study
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Viral antibodies were tested in a cohort of 44 isletcell antibody-positive individuals age 7–19 years, and 44 of their islet cell antibody-negative age and sex-matched classmates selected from a population study of 4208 pupils who had been screened for islet cell antibodies. Anti-coxsackie B1-5 IgM responses were detected in 14 of 44 (32%) of the islet cell antibody-positive subjects and in 7 of 44 (16%) control subjects. This difference did not reach the level of statistical significance. None of the islet cell antibody-positive subjects had specific IgM antibodies to mumps, rubella, or cytomegalovirus. There was also no increase in the prevalence or the mean titres of anti-mumps-IgG or IgA and anti-cytomegalovirus-IgG in islet cell antibody-positive subjects compared to control subjects. These results do not suggest any association between islet cell antibodies, and possibly insulitis, with recent mumps, rubella or cytomegalo virus infection. Further studies are required to clarify the relationship between islet cell antibodies and coxsackie B virus infections.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00408360
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  • 8
    Electronic Resource
    Electronic Resource
    Autoantibodies to ICA12 (SOX-13) are not specific for Type I diabetes (2000)
    Springer
    Diabetologia 43 (2000), S. 1381-1384 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Autoantibodies, autoantigen, ICA12, SOX-13, Type I diabetes.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Aims/hypothesis. The majority of patients with Type I (insulin-dependent) diabetes mellitus has autoantibodies to insulin, glutamic acid decarboxylase and the tyrosine phosphatase-like protein IA-2. Some patients with Type I diabetes, in particular with adult onset diabetes, have, however, only cytoplasmic islet cell antibodies that could be directed to as yet unknown beta cell autoantigens. Recently, one potential antigen, ICA12, was identified as the high mobility group (HMG) box transcription factor SOX-13. Our aim was to evaluate the diagnostic sensitivity and specificity of autoantibodies to SOX-13 for autoimmune diabetes.¶Methods. Full-length SOX-13 was cloned from human brain mRNA, expressed by vitro transcription/translation and used to detect autoantibodies by immunoprecipitation and radioligand assay in patients suffering from autoimmune diabetes or non-organ-specific autoimmune diseases.¶Results. We found SOX-13 antibodies to be present in 11 of 125 (8.8 %) patients with newly diagnosed Type I diabetes and in 3 of 43 (7.0 %) patients with latent autoimmune diabetes in adults. There was no association with age, sex and a particular pattern of diabetes-specific autoantibodies. Similar frequencies of SOX-13 antibodies were found in 84 patients with rheumatic diseases (4.0–11.4 %) and 211 healthy control subjects (5.2 %).¶Conclusions/interpretation. Our data indicate that SOX-13 represents a minor target of autoantibodies in patients with autoimmune diabetes. Because SOX-13 antibodies were found not to be disease-specific, we assume they are not helpful in improving the diagnosis and prediction of Type I diabetes. [Diabetologia (2000) 43: 1381–1384]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250051542
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  • 9
    Electronic Resource
    Electronic Resource
    Insulin autoantibodies as determined by competitive radiobinding assay are positively correlated with impaired beta-cell function — The Ulm-Frankfurt population study (1991)
    Springer
    Journal of molecular medicine 69 (1991), S. 736-741 
    Details
    ISSN: 1432-1440
    Keywords: CIAA ; CF-ICA ; Beta-cell function ; IVGTT ; HLA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Out of a random population of 4208 non-diabetic pupils without a family history of Type I diabetes 44 (1.05%) individuals had islet cell antibody (ICA) levels greater or equal to 5 Juvenile Diabetes Foundation (JDF) units. 39 of these ICA-positives could be repeatedly tested for circulating insulin autoantibodies (CIAA) using a competitive radiobinding assay. The results were compared with the insulin responses in the intravenous glucose tolerance tests (IVGTT) and with HLA types. Six pupils were positive for CIAA. All of them had complement-fixing ICA, and 5 of them were HLA-DR4 positive. Three of the 6 showed a first-phase insulin response below the first percentile of normal controls. Our data indicate that in population-based studies CIAA can be considered as a high risk marker for impaired beta-cell function in non-diabetic ICA-positive individuals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01797611
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  • 10
    Electronic Resource
    Electronic Resource
    Das Stiff-Man-Syndrom aus internistischer und immunologischer Sicht (2000)
    Springer
    Der Internist 41 (2000), S. 460-466 
    Details
    ISSN: 1432-1289
    Keywords: Schlüsselwörter ; Stiff-Man-Syndrom ; Typ 1 Diabetes ; Autoimmunerkrankung ; Glutamate Decarboxylase ; Epitope ; Th1/Th2 Immunreaktion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Zum Thema Diese Arbeit referiert im wesentlichen über den augenblicklichen Wissensstand der Ätiologie und Pathogenese des Stiff-Man-Syndroms (SMS) unter immunologischen Gesichtspunkten, während klinische und andere Aspekte in der Arbeit von H.-M. Meinck im gleichen Heft des INTERNIST eingehend behandelt werden. Auch wenn das SMS für sich gesehen wegen seiner Seltenheit vielleicht ein geringeres Leserinteresse hervorruft, ist die Verbindung zu anderen Autoimmunerkrankungen und zum Typ 1 Diabetes absolut faszinierend, handelt es sich doch beim SMS möglicherweise um die Manifestation einer autoimmunen Polyendokrinopathie. Unter diesem Blickwinkel findet die vorliegende Übersicht sicher das besondere Interesse der Leserinnen und Leser. Neben den Befunden, die Autoimmunphänomene und die Immunpathogenese des SMS betreffen, werden in kurzer Form grundsätzliche Fragen zum zellulären und humoralen Immunsystems des Körpers behandelt. Aus dem Verständnis der Autoimmunreaktion ergeben sich auch Therapieoptionen, die ebenfalls dargestellt werden.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001080050539
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