Project/Area Number |
07670547
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
内科学一般
|
Research Institution | ST.MARIANNA UNIVERSITY SCHOOL OF MEDICINE |
Principal Investigator |
SUZUKI Noboru St.Marianna University School of Medicine, Institute of Medical Science, Senior Associate Professor, 難病治療研究センター, 助教授 (40235982)
|
Co-Investigator(Kenkyū-buntansha) |
中島 敏治 聖マリアンナ医科大学, 難病治療研究センター, 助手 (70247401)
|
Project Period (FY) |
1995 – 1996
|
Project Status |
Completed (Fiscal Year 1996)
|
Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1995: ¥1,700,000 (Direct Cost: ¥1,700,000)
|
Keywords | CD28 / accessory molecule / Tlymphocytes / helper T cells / systemic lupus erythematosus / oligoclonal / activation / HLA-DR / T細胞 / アクセサリーシグナル / CD28分子 / ヘルパー機能 |
Research Abstract |
Systemic lupus erythematosus (SLE) is characterized by B cell hyperactivity and defects of immunoregulatory T cells. CD28 antigen is an accessory molecule, that transduces a potent costimulatory signal for cell activation, and is expressed on the vast majority of CD4_+ T cells. It has been reported that CD4_+CD28_- T cells were refractory to anergy induction and showed sustained reactivity to the self antigen, suggesting involvement of CD4_+CD28_- T cells in the pathogenesis of autoimmune diseases. We found that CD4_+ CD28_- T cells are prevalent in peripheral blood in patients with SLE.This T cell subset expressed HLA-DR,IL-2 receptor, VLAbeta chain brightly, indicating that this subset locates in a late stage of T cell activation cascade. We found that CD4_+ CD28_- T cells exhibited oligoclonal expansion of the selected clones. In addition, CD4_+ CD28_- T cells produced large amounts of IL-6 spontaneously. These results suggest that SLE CD4_+CD28_- T cells have been activated by unidentified, possibly self, antigen in vivo and participate in the pathogenesis of human SLE.
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