1994 Fiscal Year Final Research Report Summary
Studies on the mechanisms of autoimmune diabetes and prevension of the disease in NOD mice.
| Project/Area Number |
05454207
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | Osaka University |
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Principal Investigator |
KIKUTANI Hitoshi Osaka Univ., Inst.Mol.Cell.Biol., Assoc.Prof., 細胞生体工学センター, 助教授 (80161412)
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| Project Period (FY) |
1993 – 1994
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| Keywords | T cell / Autoimmunity / MHC class II antigen / Autoantigen / NOD mouse / Type I diabetes |
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| Research Abstract |
The following experiments were carried out using NOD mouse to elucidate the mechanisms of development of autoimmunity.
1. Self antigens recognized by 5 autoreactive T cell clones from NOD mice were characterized. All these clones reacted with antigens that were rapidly released from pancreatic islet cells. Two of these T cell clones were found to recognized distinct epitopes.
2. We also attempted to transfer diabetes to NOD-scid using T cell clones. All the clones could transfer insulitis to NOD-scid. However, diabetes could be transfered only when a mixture of these clones were injected to NOD-scid.
3. Previously, I-E transgenes could prevent diabetes of NOD mice. However, when spleen cells of I-E NOD mice were transfered to NOD-scid, development of diabetes was observed. This indicates that autoreactive T cells may exist but their activity may be suppressed in I-E NOD mice.
4. Glutamic acid decarboxylase (GAD) is one of candidates of diabetogenic antigens. To determine that GAD is really diabetogenic, GAD transgenic mice were produced.
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[Publications] Fujiwara, H., H.Kikutani, S.Suematsu, T.Naka, K.Oshida, K.Yoshida, T.Tanaka, M.Suemura, N.Matsumoto, S.Kojima, T.Kishimoto, and N.Yoshida.: "The absence of IgE antibody-mediated augmentation of immune responses in CD23-deficient mice." Proc.Natl.Acad.Sci., USA. 91. 6835-6839 (1994)
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「研究成果報告書概要(欧文)」より
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