| Project/Area Number |
01570208
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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 |
Experimental pathology
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| Research Institution | Aichi Cancer Center |
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Principal Investigator |
TAGUCHI Osamu Laboratory of Experimental Pathology, Senior Researcher, 病理学第2部, 主任研究員 (00142167)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1990: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1989: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Mouse / Thymectomy / Autoimmune disease / 胸線摘除 |
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| Research Abstract |
NZB/NZWF1 (BWF1) and MRL/Mp-1pr/1pr (MRL/1pr) mice spontaneously develop a disorder resembling human systemic lupus erythematosus (SLE). The non-obese diabetic (NOD) mouse, a model of human insulin dependent diabetes mellitus, develops autoimmune insulitis. We have been reported that spontaneous development of organ-localized autoimmune diseases, such as thyroiditis, gastritis, in day 3 thymectomized (Tx-3) standard mice such as BALB/c and A/J mice. Such autoimmune diseases does not develop in Tx-7 mice. The purpose of this investigation was to examine the role of the thymus in the various mice that spontaneously developing SLE and insulitis. Development of glomerulonephritis and polyarthritis was found in Tx-3 BWF1 and MRL/1pr mice. The incidence and severity of these lesions were almost same to those of non-Tx mice. Organ-licolized autoimmune diseases, such as gastritis and oophoritis, were found in these Tx-3 mice. Together indicating that effector T cells for induction of both systemic and organ-localized autoimmune diseases were peripheralized from the thymus at early neonatal age. Multiple development of organ-localized autoimmune diseases were found in Tx-3 NOD mice. Such autoimmune diseases were also found in Tx-7 and Tx-14 mice indicating the functional abnormality of the thymus. The incidence and severity of insulitis in Tx-3 NOD mice were lower than those of untreated mice. Post-Tx autoimmune lesions were prevented by splenic T cells with L3T4 phenotype obtained from syngeneic normal mice.
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