| Project/Area Number |
60570532
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内分泌・代謝学
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| Research Institution | OSAKA UNIVERSITY |
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Principal Investigator |
HANAFUSA TOSHIAKI OSAKA UNIVERSITY MEDICAL SCHOOL, 医学部, 助手 (60164886)
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| Co-Investigator(Kenkyū-buntansha) |
栗原 宏子 大阪大学, 医学部附属病院, 医員
TARUI SEIICHIRO OSAKA UNIVERSITY MEDICAL SCHOOL, PROFESSOR, 医学部, 教授 (00028341)
FUJINO-KURIHARA HIROKO OSAKA UNIVERSITY HOSPITAL
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1986: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1985: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | NOD mouse / Type <I> diabetes / Insulitis / Autoimmunity / T cells / B cells / NK cells / 成因 |
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| Research Abstract |
To clarify the pathogenesis of Type <I> (insulin-dependent) diabetes mellitus, non-obese diabetic (NOD) mice were studied immunologically. The results are as follows.
1. Change of cells infiltrating pancreatic islets. (1) Infiltrating cells were predominantly Thy-1+ cells (T lymphocytes), among which more Lyt- <1^+> (mainly helper/inducer) T cells were seen than Lyt- <2^+> (mainly cytotoxic/suppressor) T cells. (2) Asialo <GM1^+> cells (mainly NK cells) were found adjacent to islets.
2. Change of spleen cell subsets. (1) Increased Thy- <1^+> cells were observed at 6, 9 and 13 weeks of age. (2) <Ig^+> cells (B lymphocytes) were decreased at 6, 9 and 13 weeks.
3. Change of autoantibodies to various tissues. (1) Islet cell antibody was weakly positive in 2/6 mice just before the start of diabetes. (2) Antibodies to the apex of thyroid cells and to salivary duct were detected in more than half of the mice. (3) Anti-adrenal and anti-gastric parietal cell antibodies were negative. (4) Anti-nuclear antibodies were positive after the start of diabetes.
4. Cytotoxic effect of spleen cells against pancreatic islet cells. (1) Cytotoxic effect of NOD mouse spleen cells against NOD and C3H mouse islet cells were higher than that of control B10.GD mouse spleen cells. (2) Allokiller activity of NOD mouse spleen cells was also higher than that of the control. (3) Modified-self killer activity of NOD mouse spleen cells was similar to that of the control.
These results showed abnormalities in cellular and humoral immunity in NOD mice. Cytotoxic effect of NOD mouse spleen cells against islet cells was indicated. These findings suggest the autoimmune mechanism in the pathogenesis of diabetes in NOD mice.
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