A study on protective immunity in mice infected with Trichinella spiralis : A new role of IL-3 as Th2 amplifier in immune response to parasite infection
| Project/Area Number |
10670230
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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 | Kochi Medical School |
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Principal Investigator |
KORENAGA Masataka Faculty of Medicine, Department of Parasitology, Associate Professor, 医学部, 助教授 (00128274)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIGUCHI Yoshihisa Faculty of Medicine, Department of Parasitology, Professor, 医学部, 教授 (10037385)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2000: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Trichinella spiralis / Th2 responses / IL-3 / IL-4 / Protective immunity / Mast cells / aly mouse / Nuclear factor inducing kinase / インターフェロン・ガンマ / Th応答 / IgG1 / パイエル板 / マウス / ヘルパーT細胞 / 感染防御免疫 / 寄生線虫 |
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| Research Abstract |
Cytokine balance is a key factor for the generation of protective immunity and pathology in nematode infections. Infection with Trichinella spiralis elevates Th2 cytokines and IL-3 secretion. Our earlier work showed that (a) IL-3 advanced the timing of adult T.spiralis expulsion ; (b) IL-3 increased both mast cells in the gut and IgE production. IL-4 has been shown to be essential for switching B cells to IgE production. The above data indicate that IL-3 could affect IgE responses by stimulation of T and/or B cell functions during the infection. In the present study we have shown that IL-3 is able to enhance the production of IL-4, and that T cells able to secrete IL-4 are activated and/or induced by in vivo treatment with IL-3. Furthermore, we have analyzed protective immunity and Th2 responses in alymphoplasia mutant mice infected with T.spiralis. It has been demonstrated that alymphoplasia in aly/aly mice is caused by a point mutation in the gene encoding NF (nuclear factor) -κB- inducing kinase which is a central mediator of NF-κB activation in T and B cells. In the present study, we have suggested that aly gene is needed for the induction of protective immunity and Th2 responses in mice infected with T.spiralis.
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Report
(4 results)
Research Products
(6 results)
