| Project/Area Number |
11470031
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Tohoku University |
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Principal Investigator |
TAKAI Toshiyuki Institute of Development, Aging and Cancer, Tohoku University, Professor, 加齢医学研究所, 教授 (20187917)
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|---|
| Co-Investigator(Kenkyū-buntansha) |
小野 栄夫 東北大学, 加齢医学研究所, 助教授 (20302218)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥6,800,000 (Direct Cost: ¥6,800,000)
Fiscal Year 2001: ¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2000: ¥3,700,000 (Direct Cost: ¥3,700,000)
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| Keywords | Immunoglobulin-like Receptor / PIR / Gene Targeting / Inhibitory Receptor / Immuomodulation / Allergy / gp49 / 免疫制御 / 自己免疫疾患 / マスト細胞 / B細胞 |
|---|
| Research Abstract |
Paired immunoglobulin-like receptor (PIR)-B inhibits receptor-mediated activation signaling in vitro, while neither the physiological role nor ligand for PIR has been elucidated. PIR-B-/- mice had an increased number of peritoneal B-1 cells with age that, along with splenic B-2 cells, were hypersensitive to B cell receptor ligation. T helper (TH)2-prone humoral responses were augmented in the mutant mice upon immunization with T-dependent antigens in terms of both interleukin-4-rich/interferon-γ-poor cytokine profile and enhanced IgG1 and IgE production. Impaired maturation of dendritic cells possibly due to perturbed intracellular signaling was responsible for the skewing. Thus, PIR-B is critical for B cell suppression, DC maturation, and for balancing TH1/TH2 immune responses.
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