Analyses of regulatory mechanisms of eosinophil functions
| Project/Area Number |
03454264
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
MIKAWA Haruki Kyoto Univ., Pediatrics, Professor, 医学部, 教授 (00026866)
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| Co-Investigator(Kenkyū-buntansha) |
NAMBU Mitsuhiko Kyoto Univ., Pediatrics, Assistant Professor, 医学部, 助手 (90228114)
MAYUMI Mitsufumi Kyoto Univ., Pediatrics, Associate Professor, 医学部, 助教授 (70135581)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 1992: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1991: ¥5,100,000 (Direct Cost: ¥5,100,000)
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| Keywords | Eosinophil / differentiation / Function / Regulation / Adhesion molecule / IgG receptor / EoL cell / 好酸性顆粒 / FcαR / サイトカイン / プロテインキナ-ゼC / cAMP |
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| Research Abstract |
Eosinophils have been considered to play an important role in allergic inflammations. In order to clearify the mechanisms of growth, differentiation and activation of eosinophils, we examined (1) characteristics of eosinophilic leukemia cell differentiation factor and (2) regulatory mechanisms of expression of cell adhesion molecules and IgG receptors and chemotactic activity of eosinophils, by using human eosinophilic leukemia cell lines EoL-1 and EoL-3 and normal human eosinophils. We showed that (a) a human ATL cell line HIL-3 secretes a novel factor which induces eosinophilic differentiation of EoL-1 cells. The factor was revealed to be a glycoprotein with a molecular weight of 30-40KD, (b) EoL-1 cells acquire the responsiveness to eosinophil chemotactic factors such as PAF, fMLP and C5a through activation of protein kinase A by cyclic AMP, (c) the expression of LFA-1 and ICAM-1 on EoL-3 cells is regulated by gamma-interferon and phorbol ester through different mechanisms, (d) peripheral blood eosinophils express mainly IgG receptor II and gamma-interferon induces IgG receptor IIIB on them. Cyclic AMP suppresses the IgG receptor IIIB expression. Eosinophils induced in vitro by IL-5 from cord blood mononuclear cells are not able to be induced to express IgG receptor IIIB by gamma-interferon, and (e) EoL-1 and EoL-3 cells also express IgG receptor II and can be induced to express IgG receptor IIIB when stimulated with a combination of cAMP and gamma-interferon. These results give us important information about the mechanisms of growth, differentiation and activation of eosinophils.
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Report
(3 results)
Research Products
(21 results)
