2002 Fiscal Year Final Research Report Summary
IL-18 is essential for the development of autoimmune disease in MRL-Fas^<lpr> mice.
| Project/Area Number |
13670484
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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 | Kinki University |
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Principal Investigator |
KINOSHITA Koji Kinki University, School of Medicine, assistant professor, 医学部, 講師 (70247980)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Systemic lupus erythematosus / IL-18 / Lupus nephritis |
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| Research Abstract |
Many cytokines are increased in the kidneys undergoing autoimmune destruction in MRL-Fas^<lpr> mice. The specific cytokine known to initiate or promote kidney injury in MRL-Fas^<lpr> mice is IFN-γ. On the other hand, IL-18 is known to be a IFN-γ iuducible factor. Thus, to examine the impact of IL-18 on renal injury in MRL-Fas^<lpr> mice, I constructed a IL-18 receptor deficient strain. MRL-Fas^<lpr> mice lacking IL-18 receptor do not develop kidney pathology, or proteinuria, and survive longer. Intrarenal IFN-γ, IL-2, and IL-12 remained at normal levels compared with wild-type mice. IL-18 receptor deficient MRL-Fas^<lpr> mice do not develop autoantibodies and intrarenal IgG deposit. Our findings demonstrate that IL=18 is critical to pathogenesis of autoimmune lupus.
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