1997 Fiscal Year Final Research Report Summary
Cytotoxic mechanisms of T-lymphocytes in peripheral neuropathy
| Project/Area Number |
08670704
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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 |
Neurology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
OKA Nobuyuki Kyoto University.Department of Neurology.Assistant Professor, 医学研究科, 助手 (90252444)
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| Co-Investigator(Kenkyū-buntansha) |
AKIGUCHI Ichiro Kyoto University.Department of Neurology.Associate Professor, 医学研究科, 助教授 (30115779)
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| Project Period (FY) |
1996 – 1997
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| Keywords | Peripheral nerve / Polyneuropathy / T cell / macrophage / TNF-alpha / COX-2 |
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| Research Abstract |
We have studied the immune-mechanisms of peripheral neuropathies, focusing on the infiltration of leukocytes and the nerve degeneration. In Chronic inflammatory demyelinating polyneuropathy, the increased expression of selectins on endothelial cells may promote extravasation of lymphocytes. TNF-alpha was upregulated on macrophages adhering to myelinated nerve fibers located in demyelinating foci. Cyclooxygenase-2 (COX-2) was also shown in macrophages which appeared to destruct myelin. These results suggest that TNF-alpha and eicosanoids are associated with active demyelination.
We then examined whether COX-2 inhibitors were effective in the treatment of experimental allergic neuritis, using rat model inoculated by human P2 peptide. Both COX-2 treatments, started after disease onset and just before inoculation, ameliolated the neuritis.
In addition, we studied the molecules for tissue injury in vasculitic neuropathies. Perforin in cytotoxic T-cells, COX-2 and matrix metalloproteinase in macrophages were upregulated in vasculitic neuropathies.
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