| Project/Area Number |
62480164
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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 |
Functional basic dentistry
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| Research Institution | Kyoto University |
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Principal Investigator |
YODOI Junji Medicul Faculty of Kyoto University, 医学部, 助手 (80108993)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 1988: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1987: ¥3,900,000 (Direct Cost: ¥3,900,000)
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| Keywords | FcepsilonR2 / CD23 / IgE-binding factor / fransfectant / IL-4 / 遺伝子導入 / ILー2R / ILー4 / ILー2 / Fcεレセプター / プロモーター / IgE産生調節 / 糖鎖SV40 / 形質転換体 / 可溶性FcεR |
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| Research Abstract |
1. We found the expression of the low affinity Fc receptor for IgE (Fc epsilon F2/CD23)on HTLV-I(+) T cell line (ED) and a cell line derived from eosinophilic leukemia (EOL-3). We investigated the regulation of Fc epsilon R2/CD23 expression on a variety of hematopoitic cells including B cell line JIJOYE and monocytic cell line U937. In results, gamma-IFN could enhance the expression of Fc epsilon R2/CD23 on U937 and EOL-3, despite gamma-IFN was able to inhibit the expression of Fc epsilon R2/CD23 on IL-4 treated B cell. Although IgE or anti-Fc epsilon R2 moAb enhanced the expression of Fc epsilon R2 on cell surface, these stimulus could not increase mRNA for Fc epsilon R2. These results suggested that sccumulation of Fc epdilon R2 on cell surface was induced by addition of IgE or anti-Fc epsilon R2 moAb. But, it was clarified that mRNA for Fc epsilon R2 increased by stimulation with anti-Fc epsilon R2 moAb. All cells expressed Fc epsilon R2 released soluble Fc epsilon R2(IgE-BF), and detected by sandwich ELISA.
2. Recombinant IgE-BF was obtained from culture supernatant of transfeced mammalian cell line with Fc epsilon R2 cDNA, we clarifies that these IgE-BF have a heterogeneity in molecular weight and in function og IgE production.
3. We found that IgE production of PBI on human system was inhibited by anti-Fc epsilon R2 moAb(H107) stimulation, and that enhancement of IL-2R/_p55(Tac) expression was induced by cross-linking with H107 and goat anti-mouse IgG on fresh leukemic cells from a patient with chronic B lymphociticleukemia(B-CLL). Perspectively, function of Fc epsilon R2 as a receptor and relationship between Fc epsilon R2 and IL-2/II-2R system are much interested.
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