Role of anti-neuronal antibodies in the pathogenesis of central nervous system lupus erythematosus
| Project/Area Number |
16590996
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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 |
膠原病・アレルギー・感染症内科学
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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)
NAGAI Tatsuo Teikyo University, Internal Medicine, Assistant Professor, 医学部, 助手 (60365947)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2004: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | systemic lupus erythematosus / central nervous system / cerebrospinal fluid / anti-neuronal antibody / ribosomal P proteins / anti-glutamate receptor antibody / epitope / lupus psychosis / リボソームP蛋白 |
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| Research Abstract |
It has been demonstrated that the epitopes of ribosomal P proteins are present on the surface of human neuroblastoma cells. We explored the relationship of antibodies to the whole ribosomal P proteins (P0, P1, P2) in cerebrospinal fluid (CSF) with diffuse psychiatric/neuropsychological syndromes in systemic lupus erythematosus (SLE). CSF were obtained from 71 SLE patients (52 patients with diffuse psychiatric/neuropsychological syndromes [diffuse NP-SLE] and 19 patients with neurologic syndromes or peripheral neuropathy [focal NP-SLE]) as well as from 24 patients with non-inflammatory neurological disease. IgG antibodies to the C-terminal 22 amino acids ribosomal P synthetic peptide (anti-P_<C22>) and those to purified bovine ribosomal P proteins (P0, P1, P2) (anti-whole P) were determined by enzyme-linked immunosorbent assay, using affinity purified IgG anti-P_<C22> as standard. The concentrations of antibodies to epitopes other than the C-terminal 22 amino acids of ribosomal P protei
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ns were calculated by subtracting anti-P_<C22> from anti-whole P (anti-P_<EX.C22>). CSF anti-whole P were significantly elevated in diffuse NP-SLE compared with focal NP-SLE or control patients. By contrast, there were no significant differences in CSF anti-P_<C22> levels among the 3 groups. Of note, CSF anti-P_<EX.C22> were significantly elevated in diffuse NP-SLE compared with the other 2 groups. CSF anti-P_<EX.C22> were not significantly correlated with CSF anti-P_<C22>, but with CSF antibodies against the 9 amino acid sequence other than the C-terminal 22 amino acids. Moreover, there was no significant correlation between CSF anti-whole P or anti-P_<EX.C22> and CSF anti-neuronal cell antibodies (anti-N). These results indicate that CSF IgG antibodies to the epitopes other than the C-terminal 22 amino acids of ribosomal P proteins are associated with the development of diffuse NP-SLE. However, the data also suggest the presence of other targets against which CSF anti-N are directed, such as anti-glutamate receptor antibodies. Less
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Report
(3 results)
Research Products
(18 results)
