Breakdown of immunological tolerance by aberrant cell trafficking of B1 cells in a murine model for SLE
| Project/Area Number |
21590430
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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 |
Experimental pathology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
ISHIKAWA Sho 東京大学, 大学院・医学系研究科, 准教授 (00159691)
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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 |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | SLE / ケモカイン / B1細胞 / 免疫寛容 / 濾胞性ヘルパーT細胞 |
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| Research Abstract |
Neutralizing anti-BLC/CXCL13 monoclonal antibody effectively inhibited B1 cell migration in chemotaxis assay and administration of the antibody resulted in increased number of peripheral B1 cells in aged BWF1 mice. Therapeutic injections of the antibody to pre-lupus BWF1 mice significantly prolonged their survival compared to those by control IgG. The levels of TFH and IgG anti-DNA antibody remained unchanged in treated mice whereas IL-17 level in the serum was markedly reduced by the antibody injection. These results suggest that BLC/CXCL13 is a possible target for immunotherapy of SLE.
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Report
(4 results)
Research Products
(7 results)
