2001 Fiscal Year Final Research Report Summary
Investigation into the roles of autoantibodies in the pathogenesis of central nervous system lupus erythematosus.
| Project/Area Number |
12670438
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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 |
内科学一般
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| Research Institution | Teikyo University School of Medicine |
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Principal Investigator |
HIROHATA Shunsei Teikyo University, Internal Medicine, Associate Professor, 医学部, 助教授 (90189895)
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| Co-Investigator(Kenkyū-buntansha) |
KIKUCHI Hirotoshi Teikyo University, Internal Medicine, Assistant Professor, 医学部, 助手 (80338681)
HIROSE Naoto Teikyo University, Internal Medicine, Assistant Professor, 医学部, 助手 (60261971)
MIYASHITA Taku Teikyo University, Internal Medicine, Assistant Professor, 医学部, 助手 (00239401)
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| Project Period (FY) |
2000 – 2001
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| Keywords | SLE / CNS lupus / anti-ribosomal P antibody / monocyte / anti-lymphocyte antibody / glutamate receptor / anti-neuronal antibody / cerebrospinan fluid |
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| Research Abstract |
We examined the presence of the epitope recognized by antiribosomal P protein antibody (anti-P) on the cell surface of human immunocompetent cells in order to delineate its role in the pathogenesis of CNS lupus. Highly purified CD4+ and GD8+ T cells, monocytes, and B cells from normal healthy individuals were reacted with affinity-purified IgG anti-P, and were stained with FITC-conjugated F(ab')_2, fragment goat anti-human IgG, followed by analysis on flow cytometry with gating for viable cells by propidium iodide staining. The presence of an epitope that is antigenically related to the earboxyl-terminal 22-amino-acid sequence of ribosomal P protein was not demonstrated on the surface offreshCD4+ and CD8+ T cells, monocytes, or fresh B cells. However, the expression of the ribosomal P epitope was induced on CD4+ and CD8+ T cells after activation with immobilized anti-CD3 and on monocytes after 24h incubation with on without IFN-γ, whereas the epitope was not expressed on activated B cells. These results indicate that anti-P is an antilymphocyte' antibody, which reacts with activated T cells and monocytes but not with resting T cells, monocytes or B cells, suggesting possible direct effects of anti-P on the immune dysregulation in systemic lupus erythematosus. We could not detect significant elevation of anti-glutamate receptor antibody in cerebrospinal fluid from patients with lupus psychosis, indicating that recognized by anti-neuronal antibody.
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