Inflammation and immunological dysfunction by HTLV-1 bZIP factor in HTLV-1 associated dieases
| Project/Area Number |
22390193
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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 |
Hematology
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| Research Institution | Kyoto University |
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Principal Investigator |
MATSUOKA Masao 京都大学, ウイルス研究所, 教授 (10244138)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2012: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2011: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2010: ¥8,060,000 (Direct Cost: ¥6,200,000、Indirect Cost: ¥1,860,000)
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| Keywords | HTLV -1 / 炎症 / HBZ / Tax / HTLV-1 / レトロウイルス / HTLV-1関連疾患 / 免疫異常 / ヒトT細胞白血病ウイルス1型 / HTLV-1関連脊髄症 / 成人T細胞白血病 / 制御性Tリンパ球 / Foxp3 |
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| Research Abstract |
HTLV -1 bZIP factor (HBZ) is encoded by the minus strand of HTLV -1 provirus, and expressed in all ATL cases and HTLV-1 carriers. HBZ transgenic mice develop not only T -cell lymphomas but also inflammatory diseases. We found that overproduction of interferon-γ (IFN-γ) caused these inflammation. As a mechanism, Foxp3 expression that is induced by HBZ is unstable, which converts Foxp3+ T cells to Foxp3 - T cells with IFN-γ overproduction. HTLV -1 infected individuals have impaired cell-mediated immunity. As a mechanism of this immunodeficiency, we found that HBZ inhibited NFAT and AP-1, which leads to suppressed production of IFN-γ in CD4+ T cells.
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Report
(4 results)
Research Products
(60 results)
