| Project/Area Number |
23791087
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Hematology
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 特発性造血障害 / NKG2D免疫 / PNH / 内科 / 免疫学 / NKG2D / 造血障害 |
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| Research Abstract |
Acquired idiopathic bone marrow failure responds to immunosuppressive therapy (IST), indicating that marrow failure is immune-mediated. However, molecular pathogenesis of the immune, including on hematopoietic progenitor cells,is unknown. In the present study, we show that NKG2D-mediated immunity closely links with marrow injury in a patient with paroxysmal nocturnal hemoglobinuria. We found both that NKG2D ligands including ULBP and MICA/B were pathologically expressed on granulocytes, whereas NKG2D receptor on lymphocytes of the patient, and that IST was effective for the marrow failure. We then propose that NKG2D-mediated immunity could directly visualizeimmune condition of the marrow failure. Currently, we are confirming the NKG2D-associated immunity decides the timing of discontinuation of IST in the patient.ient.
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