Cloning of encephalitogenic T cells and analysis of immune mechanisms and treatment of experimental autoimmune encephalomyelitis.
| Project/Area Number |
60480225
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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 |
Neurology
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| Research Institution | National Center of Neurology and Psychiatry (N C N P) (1986)
国立武蔵療養所 (1985) |
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Principal Investigator |
TABIRA Takeshi National Institute of Neuroscience, National Center of Neurology and Psychiatry, その他, その他 (80112332)
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| Co-Investigator(Kenkyū-buntansha) |
KUNISHITA Tatsuhide same, 神経センター神経研究所疾病研究第6部, 研究員 (40167383)
NAMIKAWA Tadashi same, 神経センター神経研究所疾病研究第6部, 研究員 (30128061)
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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 |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 1986: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1985: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Experimental allergic encephalomyelitis / Autoimmune / Myelin basic protein / Myelin proteolipid apoprotein / Demyelination / 多発性硬化症 |
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| Research Abstract |
1. Finding of a novel encephalitogen.
It is well known that myelin basic protein (MBP) is an encephalitogen of experimental allergic encephalomyelitis (EAE). Myelin proteolipid apoprotein (PLP), a major protein component of central nerve myelin, was thought to be encephalitogenic in 1950s. However, it was denied because of contamination with MBP. This study has proven that PLP is a definite encephalitogen in guinea pigs, rats and mice. We have also shown that DM-20, a component of PLP, induces chronic relapsing EAE with widespread demyelination in BALB/c mice and T cell lines specific for PLP induce acute and relapsing EAE in SJL/J mice. These findings significantly contributed to the understanding of autoimmune encephalomyelitis especially of multiple sclerosis.
2. Analysis of immune mechanisms of EAE using T cell lines and clones.
MBP-spepcific encephalitogenic T cell lines and clones were established and used for analysis of cellular mechanism of EAE. We found that (1) a single T cell clone is enough to induce full-blown EAE in nude mice, (2) Ia antigens are expressed in the central nervous system lesions at acute and relapsed stage, and (3) an encephalitogenic T cell clone can be activated by allo-antigens and induces acute EAE.
3. Analysis of recovery mechanism and tolerance.
In order to develope new immunological treatment, we have studied recovery mechanism of acute EAE in Lewis rats. Self-limited ability of encephalitogenic T cells to continuous antigenic stimulation and environmental factors seem to be involved in the suppression. Suppression of EAE with antiserum to encephalitogenic T cell clone is now under study.
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Report
(1 results)
Research Products
(16 results)
