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  • 1
    ISSN: 1432-1440
    Keywords: Type I diabetes ; Autoimmunity ; Ia-antigen bearing cells ; ICA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Peripheral blood lymphocytes have been investigated in 20 newly diagnosed type-I diabetics and 10 healthy subjects using monoclonal antibodies. Mononuclear cells were marked with anti-T-lymphocytes (Leu2, 3, 4, 12) and anti-Ia-antibodies (K14, L243) using indirect immunofluorescence. The percentage of circulating K14- and L243-positive cells was significantly higher in all diabetics than in normal controls. An increase in the number of K14-bearing cells was found in newly diagnosed patients with duration of less than 7 days (n=10) compared with diabetics of longer duration (1 to 8 months;n=10). Using dual-color immunofluorescence with fluorescein-conjugated anti-T-lymphocytes and rhodamin-conjugated anti-Ia-antibodies it was not possible to identify Ia-antigen bearing cells (Ia cells) as helper or suppressor lymphocytes. In addition, there was no significant difference in the number of Ia cells in diabetics with and without islet cell antibodies. It is concluded that there is evidence of activation of cellular immune response in type I diabetes, particularly in the early days of manifestation. However, previous assumptions that Ia cells represent T-cell activation have to be questioned.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 31 (1988), S. 632-635 
    ISSN: 1432-0428
    Keywords: Epidermal Langerhans cells ; Type 1 (insulin-dependent) diabetes ; antigen presentation ; autoimmunity ; monocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Immunocompetent antigen-presenting Langerhans cells were investigated in skin biopsies of 20 short-term Type 1 (insulin-dependent) diabetic patients and compared with 17 matched normal control subjects. Langerhans cells in epidermal sheet preparations were visualized with a monoclonal anti-HLA DR antibody using indirect immunofluorescence. A significant decrease of Langerhans cells/mm2 body surface area was found in 10 patients immediately at the onset of diabetes compared to 10 patients with 6 months duration of diabetes and to normal control subjects (401±30 vs 559±43 vs 611±33, p〈0.01 and p〈0.002). There was no significant difference in the number of Langerhans cells between patients with 6 months duration of diabetes and control subjects. Examination of the most likely precursor of Langerhans cells, the blood monocytes, indicated an increase of monocyte counts in Type 1 diabetic patients after 6 months duration (344±37 cells/μl vs 191±31 in control subjects, p〈0.05) and an inverse correlation between the number of Langerhans cells in skin with the number of monocytes in peripheral blood (at onset: r=−0.73, p〈0.01, after 6 months of diabetes: r=−0.61, p〈0.05). In addition, a positive correlation between Langerhans cells and daily insulin dose was noted in patients after 6 months of diabetes (r=0.76, p〈0.01). The data suggest a loss of Langerhans cells in skin at the onset of Type 1 diabetes and that functional alterations of these and perhaps also other antigenpresenting cells may be involved in the pathogenesis of Type 1 diabetes.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 37 (1994), S. 1132-1141 
    ISSN: 1432-0428
    Keywords: Key words Lymphocyte subsets ; insulin-dependent diabetes mellitus ; gestational diabetes ; cord blood.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the impact of diabetic mothers on the maturation of the immune system in their offspring, immunophenotypic markers of major lymphocyte subpopulations were evaluated by two-colour flow cytometric analysis in 160 healthy children of diabetic mothers (100 with insulin-dependent diabetes mellitus (IDDM); 48 with gestational diabetes), including 22 neonates, 45 infants aged 8–12 months, 46 children aged 1–2 years, 29 children aged 3–6 years and 18 children aged 7–17 years. Results were compared with 21 neonates of healthy mothers from our hospital and with 110 paediatric subjects of a reference population. In neonates of diabetic mothers, percentages of total lymphocytes (p = 0.044), T and B lymphocytes (p = 0.004, respectively) were significantly decreased compared to our neonates of healthy mothers. By subdividing the group of neonates in offspring of mothers with IDDM (n = 15) or gestational diabetes (n = 7), differences compared to normal neonates were mainly observed in neonates of mothers with IDDM (T lymphocytes: p = 0.006; B lymphocytes: p = 0.008). In cord blood, 45.5 % of neonates had antibodies to islet cells, insulin or glutamic acid decarboxylase, most likely transmitted through the placenta of the diabetic mother. No association was found between alterations of lymphocyte subsets and antibody-positivity in cord blood, nor was there any correlation of lymphocyte counts and mean HbA1 during pregnancy, maternal age at delivery, diabetes duration, or neonatal birth weight, respectively. Comparisons among age groups from newborn infants through adolescents revealed higher percentages of total lymphocytes and lower percentages of activated T cells in children of diabetic mothers compared to children of the reference population between the age of 1 to 6 years (67–73 % of the cases above and 62–77 % below the interquartiles of the reference range, respectively). No significant differences in lymphocyte subpopulations between children of mothers with IDDM diabetes and gestational diabetes have been detected. In addition, there were no abnormalities of lymphocyte subsets in children who are at high risk for the development of IDDM. In summary, we suggest that the observed changes in children of diabetic mothers may reflect a cellular immune reaction to the particular maternal environment, characterized by both an abnormal metabolic state and persisting autoimmunity in the affected mother. [Diabetologia (1994) 37: 1132–1141]
    Type of Medium: Electronic Resource
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