| Budget Amount *help |
¥13,800,000 (Direct Cost: ¥13,800,000)
Fiscal Year 2003: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥10,400,000 (Direct Cost: ¥10,400,000)
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| Research Abstract |
In the present project, we have clarified a significance of histamine receptor-mediated signals on the regulation of acquired immune response. Since histamine is produced by mast cells, macrophages and various inflammatory cells, this is another example of regulatory mechanism of innate immunity to the acquired immunity. 1)we have shown that Th1 helper T cells preferentially express histamine H1 receptors(H1R), while Th2 cells express preferentially H2 receptors(H2R). Signals from H1R strongly up-regulates Th1 response leading to enhanced production of IFN_γ. On the other hand, histamine down-regulates Th2 responses via H2R. Subsequently, histamine, which triggers allergic reaction acting on endothelial cells, smooth muscles of blood vessels, down regulates IgE response by induction of Th1 dominance. Thus, histamine itself ceases allergic reaction as a feedback mechanism. Signals from H1R on Th1 cells enhances IFN_γ production, thus it appears to be involved in deterioration of Th1 type autoimmune diseases. On the other hand, our results clearly demonstrated that histamine strongly down regulated inflammatory responses in liver via H2R. Our results strongly indicate that histamine plays a crucial role inne receptor type 2.
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