2014 Fiscal Year Final Research Report
Analysis of Th2/17 adjuvant activities and its application
| Project/Area Number |
23591466
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Saitama Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SHIMOJO Naoki 千葉大学, 医学部, 教授 (40221303)
NAKAGOME Kazuyuki 埼玉医科大学, 医学部, 講師 (60401113)
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| Research Collaborator |
SASAKI Takumi 化学及血清療法研究所
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Keywords | アレルギー学 / アトピー性皮膚炎 / CoA / ドパミン受容体 |
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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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| Free Research Field |
医歯薬学
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