| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2003: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2000: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
A hallmark of inflammatory disease is the destruction of tissue cells by infiltrating lymphocytes, neutrophils and macrophages. The regulation of apoptosis of both target tissues and the infiltrating cells is one of the key events that defines the initiation and the progression of inflammation. We recently isolated a novel apoptosis inhibitory factor, termed AIM, which is secreted by tissue macrophages. In this report, we present unique characteristics of AIM associated with liver inflammation (hepatitis), identified by introducing an experimental fulminant hepatitis in both AIM-transgenic mice, which overexpressAIM in the body, and normal mice. AIM appears to inhibit the death of macrophages in the inflammatory regions, judging by the remarkably increased number of macrophages observed in the liver from transgenic mice. In addition, AIM also enhances the phagocytosis by macrophages. Moreover, other new functions of AIM are found. These are, AIM tempers granuloma progression by inhibiting apoptosis of T and natural killer (NK) T cells, and AIM induces growth inhibition of B lymphocytes. Based on these, we make hypothesis that AIM may also contribute to the disease progression of primary biliary cirrhosis (PBC), which is a kind of autoimmune diseases, and causes hepatitis. By in situ assay, AIM mRNA expression is upregulated at the site of inflammations in bile ducts. AIM might affect many kinds of inflammation. To study the role of AIM might be of great interest.
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