| Project/Area Number |
10670409
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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 | The University of Tokyo |
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Principal Investigator |
NAKAJIMA Toshiharu University of Tokyo, Graduate School of Medicine, Assistant professor, 大学院・医学系研究科, 寄付講座教員 (20155724)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Masao University of Tokyo Hospital, Assistant professor, 医学部・附属病院, 助手 (10302704)
MORITA Yutaka University of Tokyo Hospital, Associate professor, 医学部・附属病院, 助教授 (60107620)
HIRAI Koichi University of Tokyo, Graduate School of Medicine, Associate professor, 大学院・医学系研究科, 客員助教授 (10156630)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | IgE / high affinity IgE receptor (FcεRI) / eosinophils / mast cells / 高親和性IgE受容体(Fc_εRI) / 副腎皮質ステロイド剤 / FcεRI |
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| Research Abstract |
We investigated whether IL-4 and IgE regulate surface expression and function of FcεRI in eosinophils, as with mast cells. Eosinophils were purified from venous blood from consenting volunteers with no history of atopic diseases. Cells were cultured with IL-5, and with or without IL-4 and/or IgE at 37℃. After culture for 7 days, the surface FcεRI expression on eosinophils was analyzed by flow cytometry using anti-FcεRI mAb, CRA-1. Although peripheral blood eosinophils did not express surface FcεRI, apparent FcεRI expression (up to 1% of mast cell FcεRI levels) was observed in eosinophils cultured with both IL-4 and IgE from all donors. The combination of IL-4 and IgB was necessary for the maximal induction of surface FcεRI expression. In the presence of IL-4 and IgE, eosinophils cultured for 2 days demonstrated low but statistically significant levels of surface FcεRI, which reached to plateau after 7 days of culture. However, cross-linking of surface FcεRI by CRA-1 failed to induce the release of eosiaophil-derived neurotoxin (EDN) or leukotriene (LT) C4, or CaィイD12+ィエD1 influx in eosinophils cultured for 7 days with IL-4 and IgE. These results suggest that surface FcεRI expression in eosinophils is regulated by a mechanism similar to that in mast cells.
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