| Project/Area Number |
17591184
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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 |
Dermatology
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| Research Institution | Kyorin University |
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Principal Investigator |
MIZUKAWA Yoshiko Kyorin University, School of Medicine, Department of Dermatology, Assistant (50301479)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | immediate-type hvpersensitivity response / IgE / TLR / mast cell / TgE / マウスモデル |
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| Research Abstract |
Although the innate immune system needs a negative feedback mechanism to ameliorate its own tissue-damaging effects, the signals and receptors that regulate mast cell functions during innate immune responses remain to be defined. We demonstrated that repeated elicitation of contact hypersensitivity (CH) in the ear resulted in the development of IgE-dependent immediate-type hypersensitivity response (ITR) mediated by mast cell degranulation: while when elicited in the footpad, IgE-independent, TLR2-mediated ITR responses emerged in mice with no detectable IgE. Because
1. There was an inverse relationship between the magnitude of ITR and the serum IgE levels as observed in the footpad.
2. A marked increase in this footpad swelling occurred in B cell deficient (μMT) mice but not in TNP-specific IgE transgenic mice.
3. The ITH responses were observed in wild-type (WT) mice, but not in TLR-2-/- mice.
4. This response is elicited in the footpad of Kit^W/Kit^<W-V> mice reconstituted with wild type-derived, but not TLR2^<-/->-derived, cultured mast cells (BMMCs) and is inhibited only when the BMMCs are pretreated with IgE.
These results indicate that IgE/FcεRI pathway may have evolved to limit the potentially harmful effects of innate immune responses.
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