| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Outline of Final Research Achievements |
We previously showed that dopamine-mediated cAMP elevation in human naïve CD4 T cells was completely inhibited by treatment with a D1-like receptor antagonist SCH-23390, which inhibited dopamine-mediated IL-6/17 secretion from T cells. We studied the effect of SCH-23390 with the SCID mice in which active RA synovial tissue and cartilage have been engrafted. Retraction of synovial tissue was observed in the SCH-23390-treated group. It was also effective in OVA-induced neutrophilic airway inflammation. Mothers, whose children developed atopic dermatitis (AD), often demonstrate a higher Th2 adjuvant activity in their milk. We showed that this is attributable to Coenzyme A (CoA), which exhibited Th2 adjuvant activity both in vitro and in vivo. Furthermore, the oral administration of CoA induced AD-like skin in mice. These data indicate that some of the patients with AD were exposed to Th2 adjuvant via mothers’ milk with high CoA content.
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