Myeloid-associated immunoglobulin-like receptors, CD300 are promising antibody-therapeutic targets for sepsis
| Project/Area Number |
21390481
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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 |
Emergency medicine
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| Research Institution | University of Tsukuba |
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Principal Investigator |
TAHARA Satoko 筑波大学, 医学医療系, 助教 (20360589)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥17,680,000 (Direct Cost: ¥13,600,000、Indirect Cost: ¥4,080,000)
Fiscal Year 2011: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2010: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2009: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | 救急蘇生学 / 敗血症 / 抗体療法 / CD300a / CD300d / エンドトキシンショック / MAIR-I / MAIR-II / TLR4 / 盲腸結紮穿孔法 / 敗血症モデル |
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| Research Abstract |
An appropriate activation of innate immune responses is crucial for control microbe infection. An excessive activation and dysfunction of innate immune responses leads to onset of sepsis. To elucidate the regulatory mechanism of innate immune responses is critical for establish the therapeutic approaches for sepsis. We have recently identified myeloid-associated immunoglobulin-like receptors, such as MAIR-I (CD300a) and MAIR-II (CD300d), and found that these receptors are crucial for regulating innate immune responses. Furthermore, administration of a monoclonal antibody against MAIR-I prolonged the survival of mice after cecal ligation and puncture (CLP)-induced sepsis.
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Report
(4 results)
Research Products
(41 results)
