| Project/Area Number |
20790699
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Nihon University |
|---|
Principal Investigator |
NUNOMURA Satoshi Nihon University, 医学部, 助教 (70424728)
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| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | マスト細胞 / 免疫学 / 病理学 / FcR / 関節リウマチ / Fc受容体 |
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| Research Abstract |
Mast cells (MCs) harboring IgG receptor contribute to the pathogenesis of rheumatoid arthritis. IgG receptor on MCs, but not on other immune cells, is expressed as a tetramer including Fc receptor β chain (FcεRIβ). However, role of FcεRIβ in the development of rheumatoid arthritis is largely unknown. In the present study we investigated the function of FcεRIβ, a regulator of IgG receptor signaling, in rheumatoid arthritis employing an anti-type II collagen (CII) Ab-induced arthritis model. FcεRIβ-/-mice exhibited increased severity of arthritis compared with WT mice. Consistent with this observation, histopathological analyses revealed that infiltrated lymphocytes into the synovium were more increased in FcεRIβ-/- mice than in WT mice. Our findings of the present study suggest that FcεRIβ plays important roles in the regulation of inflammatory responses and that it act as an inhibitory molecule in the development of arthritis.
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