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  • 1
    Electronic Resource
    Electronic Resource
    Spontaneous autoimmune reactions against pancreatic islets in mouse strains with generalized autoimmune disease (1980)
    Springer
    Diabetologia 19 (1980), S. 216-221 
    Details
    ISSN: 1432-0428
    Keywords: Insulitis ; abnormal glucose tolerance ; NZB mice ; autoimmune mouse strains ; cellular autoimmunity ; diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The spontaneously autoimmune mouse strains NZB, NZB x NZW, MRL and BXSB have been examined for signs of autoimmune reactions against islet cells. Between 15 and 55 animals of each strain were tested. Infiltrates of lymphocytes and fibroblasts into pancreatic islets were found in more than 80% of NZB mice, in about 50% of MRL and NZB x NZW mice, and in less than 20% of BXSB mice. Infiltrates were not found in the exocrine portion of pancrea. All NZB mice had abnormal glucose tolerance. In the three other strains between 20 and 50% of animals had abnormal glucose tolerance. All mice had fasting normoglycaemia. The lesions in NZB mice were studied in more detail. It was found by ultrastructural analysis that in young mice pancreatic infiltrates consisted of lymphocytes and fibroblasts. Single lymphocytes were also seen outside the main infiltration area. After 2 to 5 months of age another type of infiltrate, consisting of lymphocytes and macrophages was observed. B-cell destruction by lymphocytes was apparent in both young and adult NZB mice. It is concluded that cellular autoimmune reactions against pancreatic islets may occur spontaneously as a consequence of immunological disorders in NZB, NZB x NZW and MRL mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00275272
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Low-dose streptozotocin-induced autoimmune diabetes is under the genetic control of the major histocompatibility complex in mice (1982)
    Springer
    Diabetologia 23 (1982), S. 69-71 
    Details
    ISSN: 1432-0428
    Keywords: H-2 dependence ; experimental autoimmune diabetes ; streptozotocin ; genetic control ; mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In mice, an experimental autoimmune diabetes can be induced by multiple injections with low doses of streptozotocin. Since different mouse strains show a varying susceptibility towards this treatment, we have examined whether the experimental autoimmune diabetes is under the genetic control of the major histocompatibility complex (H-2 complex). Mice of five congenic resistant strains, differing in their genome only at the H-2 region, were identically treated on five consecutive days with 40 mg streptozotocin/kg body weight. Genes at the H-2 complex were found to determine the susceptibility towards the diabetogenic effect of streptozotocin: mice of H-2 haplotype k (B10.BR) developed persistent and strong hyperglycaemia (blood glucose approximately 17 mmol/1), mice of strain B10.A (H-2a), C57BL/10 (H-2b) and B10.D2 (H-2d) reacted with moderate hyperglycaemia (between 11.5 and 15.5 mmol/1), whereas mice of strain B10.S (H-2s) were resistant to the diabetogenic effect of low-dose streptozotocin except for a small and transient rise of blood glucose levels. It is concluded that genes within the major histocompatibility complex affect the diabetogenic response to multiple low-dose streptozotocin treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00257735
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Transfer of experimental autoimmune insulitis by spleen cells in mice (1980)
    Springer
    Diabetologia 19 (1980), S. 516-520 
    Details
    ISSN: 1432-0428
    Keywords: Insulitis ; lymphocyte transfer ; cellular immunity ; streptozotocin ; experimental diabetes mellitus ; glucose intolerance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have tested whether experimental insulitis induced by multiple subdiabetogenic injections of streptozotocin can be transferred by lymphocytes to normal recipients. C57BL/6J mice were treated on 5 consecutive days with 40 mg streptozotocin /kg body weight. 5×107 nucleated spleen cells from 20 animals which had developed hyperglycaemia with concomitant insulitis three weeks after the first streptozotocin-injection, were transferred into congenic thymusless C57BL/6J-nu/nu mice. The cell transfer led to lymphocytic infiltrations of pancreatic islets in 75% of the recipients. Hyperglycaemia was not observed. It is concluded that lowdose streptozotocin treatment induces cellular immune reactions against pancreatic islets.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00253178
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Pathogenesis of low dose streptozotocin induced diabetes in mice: requirement for α1-adrenoceptor activation and vasoactive amine release (1989)
    Springer
    Diabetologia 32 (1989), S. 140-142 
    Details
    ISSN: 1432-0428
    Keywords: Streptozotocin (low dose) ; prazosin ; vasoactive amine antagonists ; insulitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Pancreatic islet inflammation and subsequent diabetes was induced by multiple low doses of streptozotocin in male C57 Bl/6J mice. The development of hyperglycaemia was almost completely prevented by treating the animals with the α1-adrenoceptor antagonist prazosin (20 mg·kg−1. day−1) as well as by the vasoactive amine antagonists methysergide (50 mg·kg−1·day−1), disodium cromoglycate (100mg·kg−1·day−1), pizotifen (5 mg·kg−1·day−1) or cyproheptadine (20 mg·kg−1·day−1). Treatment with vasoactive amine antagonists largely inhibited infiltration of pancreatic islets by L3T4+-lymphocytes and to a lesser extent by Lyt2+-cells. The infiltration of macrophages was not affected except after pizotifen treatment. These results indicate that α1-adrenoceptor activation is required for disease development and that vasoactive amine release is a prerequisite for lymphocytic insulitis but not for macrophage infiltration of islets.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00505187
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Modulation of low-dose streptozotocin-induced diabetes in mice by administration of antibodies to I-A, I-E and I-J determinants (1989)
    Springer
    Diabetologia 32 (1989), S. 173-176 
    Details
    ISSN: 1432-0428
    Keywords: Experimental diabetes ; mice ; streptozotocin ; anti-Ia-antibodies ; major histocompatibility complex ; immunomodulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In male mice of strains C3H and C57BL/6 an experimental immune-mediated diabetes can be induced by multiple low doses of streptozotocin. The delay and partial suppression of hyperglycaemia after anti-I-A monoclonal antibody administration was dose dependent. Even saturation levels of anti-I-A did not cause complete protection from diabetes development. Administration of anti-I-E monoclonal antibody also significantly delayed the onset of hyperglycaemia. Surprisingly, the combined treatment with anti-I-A and anti-I-E did not result in better protection from diabetes. Thus, there is an I-A and I-E independent component of the disease. Furthermore, there is no restriction to either I-A or I-E. Anti-I-A was only effective when given at the beginning of the experiment, which implies that I-A molecules have a primary function during the induction of diabetes. The contribution of I-J to the disease process is different. Administration of a polyspecific alloantiserum to I-J almost completely prevented hyperglycaemia. Injections of monospecific antibodies to I-J determinants enhanced hyperglycaemia, especially when given after the induction of diabetes. This indicates that I-J is involved in initial as well as in later stages of the disease process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00265090
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    Paper (German National Licenses)
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