| Project/Area Number |
61480158
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | Osaka University |
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Principal Investigator |
TANIGUCHI TADATSUGU Institute for Molecular and Cellular Biology, Osaka University, 細胞工学センター, 教授 (50133616)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA GEN Institute for Molecular and Cellular Biology, Osaka University, 細胞工学センター, 助手 (80174712)
FUJITA TAKASHI Institute for Molecular and Cellular Biology, Osaka University, 細胞工学センター, 助手 (10156870)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥6,200,000 (Direct Cost: ¥6,200,000)
Fiscal Year 1987: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1986: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | Interleukin-2 / Lymphokine / Il-2 Receptor / ATL / 成人性T細胞白血病 / 成人T細胞白血病 / リンフォカイン / 遺伝子発現 |
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| Research Abstract |
Interleukin-2 (IL-2) is a lymphokine which plays a key role in T cell growth and differentiation. We performed a series of studies in order to analyze molecular regulatory mechanism of IL-2 gene expression and T cell growth control which is mediated by the IL-2 system.
We cloned and analyzed the 5' flanking sequences of human IL-2 and IL-2 receptor (p55,Tac) gene and we identified functional DNA sequences controlling the IL-2 and IL-2R gene expression at the transcriptional level in activated T cells.
IL-2 system has also been studied in relation to the development of adult T cell leukemia/lymphoma (ATL). Our studies revealed that distinct DNA sequences of the 5' flanking region of IL-2 and IL-2R genes are responsible for the transcriptional activation by tat I (p40^x) protein which is encoded by HTLV-1. Furthermore, we showed that IL-2 gene is synergistically activated by tat I (p40^x) and extracellular stimulation mediated by T3/Ti complex. So the next emerging problem is to examine whether operation of IL-2 autocrine growth stimulation actually contributes to the generation of tumorigenic T cells or not. We constructed a recombinant retroviral Vector for IL-2 production in various cells, and by utilizing the virus we obtained results suggesting further the importance of aberrant operation of the IL-2 autocrine loop in the development of T cell marignancy.
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