1997 Fiscal Year Final Research Report Summary
Analysis of IgE production in vivo by CD1-specific CD4+NK 1.1+T cells and IGIF.
| Project/Area Number |
08839022
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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 |
免疫の制御機構
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| Research Institution | Hyogo College of Medicine |
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Principal Investigator |
YOSHIMOTO Tomohiro Hyogo College of Medicine, Department of Immunology and Medical Zoology, Lecture, 医学部, 講師 (60241171)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMURA Haruki Hyogo College of Medicine, Laboratory of Host Defenses, Institute for Advanced M, 医学部, 助教授 (60111043)
NAKANISHI Kenji Hyogo College of Medicine, Department of Immunology and Medical Zoology, Profess, 医学部, 教授 (60172350)
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| Project Period (FY) |
1996 – 1997
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| Keywords | NK1.1+cells / IGIF (IL-18) / IL-12 / IL-18 receptor / IgE / SJL mice |
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| Research Abstract |
We have presented that mouse CD-1-specific CD4+NK1.1+T cells that produce IL-4 promptly upon in vivo stimulation, are essential for the induction of IL-4-producing cells and for switching to IgE,an IL-4-dependent event. We further showed that Propionibacterium acnes treatment diminishes CD4+NK1.1+T cells but induces type 1 T cells in the liver by induction of IL-12 and IL-18 production from kupffer cells (J.Immunol. 1997). These CD4+NK1.1+T cells diminished mice produced low levels of IgE.Recently, we showed that a combination of IL-12 and IL-18 induce anti-CD40-activated B cells to produce IFNg, which inhibits IL-4-dependent IgE production, suggesting that B cells can act as regulatory cells (PNAS,1997). As B cells require co-stimulation with IL-12 to produce IL-18 by striking IFNg production, we investigated IL-18 receptor (IL-18R) expression on B cells. We also demonstrated that T cell-depleted B cells from SJL mice, which are known for their genetically poor ability to produce IgE upon helminth infection, fails to produce IgE following stimulation with LPS and IL-4 in vitro, due to the action of IL-12 and IL-18 produced by contaminating macrophages. Furthermore, we demonstrated that IL-18 and IL-12 from LPS-stimulated macrophages synergistically induce unique T cells (CD3intIL-2Rbeta+T cells) to secrete IFNg and to express Fas ligand, which in combination inhibits IgE production from B cells (J.Immunol. in press ). Thus administration of IL-12 and IL-18 could present a unique approach for the treatment of allergic disorders.
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[Publications] Matsui, K., Yoshimoto, T., Tsutsui, H., Hyodo, Y., Hayashi, N., Hiroishi, K., Okamura, H., Nakanishi, K.and Higashino, K.: "Propiobacterium acnes treatment diminishes CD4+NK1.1+T cells but induces type 1 T cells in the liver by induction of IL-12 and IL-18." J.Immunol.159. 97-106 (1997)
Description
「研究成果報告書概要(欧文)」より
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[Publications] Takeda, K., Tsutsui, H., Yoshimoto, T., Adachi, O., Yoshida, N., Kishimoto, T., Okamura, H., Nakanishi, K.and Akira, S.: "Defective NK cell activity and Th1 response in IL-18-deficient mice." Immunity.(In press). (1998)
Description
「研究成果報告書概要(欧文)」より
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