2012 Fiscal Year Final Research Report
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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| Keywords | HTLV -1 / 炎症 / HBZ / Tax |
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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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[Journal Article] HTLV-1 bZIP factor induces T-cell lymphoma and systemic inflammation in vivo2011
Author(s)
Satou Y, Yasunaga J, Zhao T, Yoshida M, Miyazato P, Takai K, Shimizu K, Ohshima K, Green PL, Ohkura N, Yamaguchi T, Ono M, Sakaguchi S, Matsuoka M
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Journal Title
PLoS Pathog
Volume: 7
Pages: 1001274
DOI
Peer Reviewed
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