| Project/Area Number |
04670398
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内科学一般
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| Research Institution | St.Marianna University School of Medicine |
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Principal Investigator |
SUZUKI Noboru St.Marianna University School of Medicine, Institute of Medical Science, Associate professor, 難病治療研究センター, 講師 (40235982)
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| Co-Investigator(Kenkyū-buntansha) |
SAKANE Tuyoshi St.Marianna University School of Medicine, The Medical Department, Professor, 医学部, 教授 (40127519)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1992: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Dehydroepiandrosterone / Systemic lupus erythematosus / Interleukin 2 / Therapy / mRNA / T lymphocytes / CD4+ T cells / IL-2 / IL-2mRNA |
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| Research Abstract |
Principal cause of the IL-2 deficiency, a common feature of both murine lupus and human systemic lupus erythematosus(SLE) remain obscure. Recent studies of our own as well as others have shown that dehydroepiandrosterone(DHEA), an intermediate compound in testosterone synthesis, significantly upregulates IL-2 production of T cells and that administration of exogenous DHEA or IL-2 via a vaccinia construct to murine lupus dramatically reverses their clinical autoimmune diseases. Thus, we have examined serum levels of DHEA in patients with SLE to test whether abnormal DHEA activity is associated with the IL-2 deficiency of the patients. We found that nearly all of the patients examined have very low levels of serum DHEA.The decreased DHEA levels are not simply a reflection of a long term corticosteroid treatment which may cause adrenal atrophy, since serum samples drawn at the onset of disease, which are devoid of corticosteroid treatment also contained low levels of DHEA.In addition, exogenous DHEA restored impaired IL-2 production of T cells from patients with SLE in vitro. These results indicate that defects of IL-2 synthesis of patients with SLE are at least in part due to the low DHEA activity in the serum.
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