2002 Fiscal Year Final Research Report Summary
Mechanisms of atopic status in Id2-deficent mise and their application to therapeutic strategy
| Project/Area Number |
13670799
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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 |
Pediatrics
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
KUSUNOKI Takashi Assistant Professor, 医学研究科, 助手 (00303818)
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| Co-Investigator(Kenkyū-buntansha) |
YOKOTA Yoshifumi Fukui Medical School, Professor, 教授 (50222386)
NAKAHATA Tatsutoshi Professor, 医学研究科, 教授 (20110744)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Id2 / Th1 / Th2 / allergy / IgE / atopy |
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| Research Abstract |
Mechanisms far atopic states found in Id2-deficient mice was investigated, and the following results were found.
1. Th1/Th2 induction of naive T cells: There was no significant difference in Th1/Th2 differentiation ability between naive CD4+T cells from control and Id2-deficient mice, indicating that there is no intrinsic defect of T cell differentiation in these mice.
2. Antigen presenting cells is Id2-deficient mice: CD11c+ dendritic cells (DC) were analyzed and found that the number of CD8+ DC, which is known to induce Th1 differentiation, was dramatically reduced in these mice.
3. IgE class-switch in B cells: B cells from Id2-deficient mice showed elevated production of IgE. Enhanced IgE class-switch was observed by germline transcription and S-S recombination analysis. Furthermore, molecular analysis showed that Id2 was induced by TGF-beta and inhibited excess IgE class-switch in B cells.
In summary, by analysis of Id2-deficient mice, we found that Id2 works as a molecular safeguard system against hyper-atopic status, by at least two mechanisms; 1)regulation of DC differentiation 2)regulation of IgE class-switch.
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