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  • 1
    Electronic Resource
    Electronic Resource
    Evidence that the reduced number of natural killer cells in Type 1 (insulin-dependent) diabetes may be genetically determined (1987)
    Springer
    Diabetologia 30 (1987), S. 907-911 
    Details
    ISSN: 1432-0428
    Keywords: Natural killer cells ; identical twins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Viruses may cause Type 1 (insulin-dependent) diabetes. We wondered whether the number and function of natural killer cells, which are important in anti-viral defense, are disturbed in diabetic patients. We studied 16 recently diagnosed Type 1 diabetic patients, 18 Type 1 diabetic patients diagnosed more than 15 years previously, 18 Type 2 (non-insulin-dependent) diabetic patients and 23 control subjects. We determined the number of natural killer cells (expressed as log10%) using anti-Leu 11 monoclonal antibody and the function (in log10 lytic units) concurrently using a 51Cr release assay with K 562 as target cells. We found that the number of natural killer cells was reduced in Type 1 diabetes (1.01±0.04) as compared with Type 2 diabetic patients (1.16±0.04, p=0.004) and normal control subjects (1.16±0.04, p=0.006). To establish whether the reduced natural killer cell number is genetically determined we studied 19 identical twin pairs discordant for Type 1 diabetes; we found that even the non-diabetic co-twins had a reduced natural killer cell number (0.93±0.05, p= 0.0006) as compared with normal control subjects. Natural killer cell function was similar in all groups while natural killer activity per cell was significantly increased in the recently diagnosed diabetic patients (1.63±0.07) as compared with long-standing diabetic patients (1.26±0.26, p= 0.03) and controls subjects (1.36±0.07, p= 0.006). In conclusion the reduced number of natural killer cells in Type 1 diabetes appears to be genetically determined while their activity at diagnosis is increased.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00295872
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  • 2
    Electronic Resource
    Electronic Resource
    Cytokine overproduction in healthy first degree relatives of patients with IDDM (1998)
    Springer
    Diabetologia 41 (1998), S. 343-349 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin-dependent diabetes mellitus ; first degree relatives of diabetic patients ; cytokines.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Healthy family members of patients with insulin-dependent diabetes mellitus (IDDM) are known to share a number of immunological abnormalities with their affected relatives. Since monocyte and type 1 T-cell-derived cytokines contribute to the pathogenesis of IDDM, we studied the production of these cytokines in the healthy first degree relatives of 29 children with IDDM. We report that circulating tumour necrosis factor-α (TNF-α) and soluble interleukin-2 (sIL-2) receptor were present in increased amounts in non-diabetic family members at levels similar to those found in the diabetic children (duration of disease 3 months–5 years). Furthermore, marked hypersecretion of IL-1α and TNF-α by mitogen-stimulated peripheral blood mononuclear cells was found in both diabetic and healthy family members. Abnormalities of cytokine production in healthy relatives did not correlate with the presence of islet cell antibodies or with HLA DR type. These data indicate that healthy family members of patients with IDDM exhibit overproduction of a number of cytokines that have been implicated in diabetogenesis. [Diabetologia (1998) 41: 343–349]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050913
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Elevated serum levels of macrophage-derived cytokines precede and accompany the onset of IDDM (1996)
    Springer
    Diabetologia 39 (1996), S. 60-69 
    Details
    ISSN: 1432-0428
    Keywords: Cytokines ; T helper subsets ; interleukin-2 ; interferon-γ ; interleukin-1 ; tumour necrosis factor ; prediabetes ; identical twins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To determine whether cytokines could have a role in the development of insulin-dependent diabetes mellitus (IDDM), we measured serum levels of cytokines derived from T helper 1 (interleukin-2 and interferon-γ), T helper 2 (interleukin-4 and inter-leukin-10) lymphocytes and macrophages (tumour necrosis factor-α, interleukin-1 α and interleukin-1 Β) in patients before and after the onset of IDDM. Recently diagnosed IDDM patients had significantly higher levels of interleukin-2, interferon-γ, tumour necrosis factor-α and interleukin-1 α than patients with either long-standing IDDM, non-insulin-dependent diabetes (NIDDM), Graves' disease, or control subjects (p〈0.05 for all). Compared with control subjects, patients with long-standing IDDM and those with NIDDM had higher interleukin-2 and tumour necrosis factor-α levels (p〈0.01 for all). Interleukin-4 and interleukin-10 were detectable in sera of patients with Graves' disease only, while interleukin-1 Β was not detectable in the serum of any control or test subject. To investigate whether high cytokine levels precede the onset of IDDM, we studied 28 non-diabetic identical co-twins of patients with IDDM, followed-up prospectively for up to 6 years after the diagnosis of the index. Levels of tumour necrosis factor-α and interleukin-1 α were elevated above the normal range more frequently in the eight twins who developed diabetes than in those 20 who did not (p〈0.005). Analysis of T helper 1 and T helper 2 profiles of the twin groups did not reveal a clear difference between prediabetic twins and twins remaining non-diabetic. These results support the notion that T helper 1 lymphocytes may play a role in the development of IDDM. This is associated with release of macrophage-derived cytokines, which is also a feature of the prediabetic period. The lack of evidence of a dominant T helper 1 profile of cytokine release before diabetes onset suggests that additional events, activating this arm of the cellular immune response, are required in the immediate prediabetic period.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400414
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Lymphocyte vaccination protects prediabetic non-obese diabetic mice from developing diabetes mellitus (1997)
    Springer
    Diabetologia 40 (1997), S. 1388-1395 
    Details
    ISSN: 1432-0428
    Keywords: Keywords T lymphocytes ; lymphocyte vaccination ; NOD mouse ; autoimmune diabetes ; immunotherapy.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the therapeutic manoeuvre termed “lymphocyte vaccination”, activated lymphocytes capable of transferring an autoimmune disease are instead attenuated and given in vaccine form. We have previously shown that such a therapy administered to non-obese diabetic (NOD) mice at 6 weeks of age prevents diabetes mellitus. To assess whether this therapy has potential clinical relevance, in the present study lymphocyte vaccination was applied in NOD mice in 3 weekly doses commencing in the immediate prediabetic period (age 12 weeks), when insulitis is advanced and diabetes incipient. Of 30 NOD mice receiving active vaccine (composed of attenuated lymphocytes from diabetic NOD mice) 13 (43.3 %) remained non-diabetic to the age of 30 weeks, in comparison with 2 of 30 (6.7 %; p 〈 0.01) mice receiving a control vaccine (composed of attenuated lymphocytes from non-diabetic NOD/B10 mice) and 5 of 26 (19.2 %; p 〈 0.01) mice receiving saline carrier alone. Moreover, in an additional group of 10 NOD mice receiving active vaccine weekly between 12 and 30 weeks, 8 remained diabetes free at the end of the treatment. The most notable effect of the vaccine was that the delay in diabetes onset was accompanied by a reduction in insulitis and in some cases a complete absence of infiltrating lymphocytes at 30 weeks of age. Immunocytochemistry indicated that when present, islet infiltrating lymphocytes in non-diabetic mice that received active vaccine showed significantly reduced staining for interferon-γ, compared with the infiltrate seen in diabetic mice receiving the control vaccine or saline. This study demonstrates that the rapid progression to diabetes typically seen in 12-week-old NOD mice can be delayed by lymphocyte vaccination, supporting the possibility that a vaccine composed of attenuated autologous peripheral blood lymphocytes could be effective in high risk first degree relatives of patients with insulin dependent diabetes mellitus. [Diabetologia (1997) 40: 1388–1395]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050840
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