| Project/Area Number |
10670218
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
YAMSUMIZU Ryoji Kansai Med. Univ., Faculty of Med., Assistant Profesor, 医学部, 助教授 (00142753)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | lpr gene / MRL / lpr mouse / lymphadenopathy / aly gene / ALY mouse / alymphoplasia / Thy1コンジェニックマウス |
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| Research Abstract |
Why the mice with the mutant lpr gene develop massive lymphadenopathy? Where and how lpr-T lymphocytes emerge and accruniliate? Why ALY mice do not develop lymph node and Peyer's patch? To address these tundamental questions, several lines of investigation have been performed, such as natural history of lpr-lynrphadenqpathy, pathophysiolagy of ALY mice, and lymph node- or bone marraw-transplautation. From the series of observations, forrowing conciusions were drawn.
・ The narural history of lpr-lymphadenopathy is much more complex than lasually thought
・ The emergence and develpment of lpr-T lymphocytes and lpr-lyntphadenopathy may reflect the dynamics of cell society under the developmental control.
・ Both lpr and aly genes must be invoived in this tempo-spatial controi on the deveiqpment of lymph node, and the mutation these genes must disrupt the normal deveipment and/or homeostasis of lymph node.
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