1998 Fiscal Year Final Research Report Summary
Regulation of polyclonal IgE production and supressor mechanisms of Th2 ifilarial parasite infection
| Project/Area Number |
09670254
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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 |
寄生虫学(含医用動物学)
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
FUJITA Koichiro Faculty of Medicine, Professor, 医学部, 教授 (90053107)
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| Co-Investigator(Kenkyū-buntansha) |
今井 伸二郎 日清製粉(株)創薬研究所, 主任研究員
TSUKIDATE Setsuko Faculty of Medicine, Instructor, 医学部, 助手 (40121256)
AKAO Nobuaki Faculty of Medicine, Lecturer, 医学部, 講師 (00126559)
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| Project Period (FY) |
1997 – 1998
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| Keywords | nonspecific IgE / Th2 / Dirofilaria immitis / Cytokine / IL-10 / B1 cell |
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| Research Abstract |
The filarial parasite infections induced high levels of serum lgE.However, the mechanisms of this phenomenon have not yet been fully elucidated. We have previously reported that the recombinant Dirofilaria immitis-derived protein(DiAg) induced polyclonal lgE production in BALB/c mice, and clarified that the responder cells to DiAg were B cell.
In this experiment, we investigated the mechanisms of polyclonal lgE production by cytokine production and studied the surface molecule expression. The production of IgE, in vitro, was significantly enhanced when restinng splenic B cells were stimulated with the combination of DiAg plus lL-4, but not DiAg alone. DiAg up-regulated the expression of CD23 on splenic B cells in vivo as well as in vitro. Expression of lL-6 and iL-10 mRNAs was relatively higher in DiAg-treated B cells as compared with untreated controls. These results suggested that DiAg enhanced IgE synthesis by inducing autocrine production of lL-6, lL-lO and by directly up-regulating CD23 expression on B cells. Then we were cleared that lL-2 production of Jurkat cells and activated T cells increased with stimulation of DiAg component. DiAg showed various actions as same as cytokine against the host immune systems.
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