Project/Area Number |
02670355
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Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
Neurology
|
Research Institution | Tohoku University |
Principal Investigator |
OHARA Yoshiro (1991) Tohoku University School of Medicine Department of Neurological Sciences Associate Professor, 医学部, 助教授 (50203914)
照沼 裕 (1990) 東北大学, 医学部, 助手 (50217436)
|
Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Teiji Fukusima Medical College Department of Neurology Professor, 教授 (10106487)
IWASAKI Yuzo Tohoku University School of Medicine Department of Neurological Sciences Profess, 医学部, 教授 (00142927)
大原 義朗 東北大学, 医学部, 助教授 (50203914)
|
Project Period (FY) |
1990 – 1991
|
Project Status |
Completed (Fiscal Year 1991)
|
Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1991: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1990: ¥1,500,000 (Direct Cost: ¥1,500,000)
|
Keywords | Major histocompatibility complex class II / Wallerian degeneration / Microglia / Experimental allergic encephalomyelitis / EAE / 脱髄 / Ia抗原 |
Research Abstract |
To clarify the Implication of the major histocompatibility complex class II(Ia)antigen Induction In microglia following the Wallerian degeneration in the central nervous system(CNS), experimental allergic encephalitis(EAE)was adoptively transferred to Lewis rats In which Ia antigens had been Induced in microglia at the sites of Wallerian degeneration. In addition, to randomly distributed typical EAE lesions, the recipient rats developed distinct inflammatory lesions In accord with the distribution of Ia-positive microglia ; l. e., In the ipsilateral thalamus after cortical injury, and In the Ipsilateral optic nerve, the contralateral optic tract and superlor colliculus after unilateral eye ball enucleation. Thus, the EAE locus may be targeted by this approach. When examined using monoclonal antibody surface markers of lymphocytes, the types of lymphocytes did not differ from those In ordinary EAE lesions In the spinal cord. The potential role of nonlmmunologically induced Ia-positive cell clusters that serve as a target for autoimmune CNS diseases was discussed.
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