Analysis of HTLV-1 bZIP factor induced inflammatory diseases

2016 Fiscal Year Final Research Report

• Project/Area Number: 25293219
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Hematology
• Research Institution: Kyoto University
• Principal Investigator: Matsuoka Masao 京都大学, ウイルス・再生医科学研究所, 客員教授 (10244138)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: HTLV-1 / HBZ / 炎症 / TIGIT / CCR4

Outline of Final Research Achievements

In this study, we found that HTLV-1 bZIP factor (HBZ) induced unstable expression of Foxp3, which is associated with overproduction of interferon-γ (IFN-γ). IFN-γ production is likend with oncogenesis and inflammation. In addition, HBZ induced GATA3 transcription, which promoted CCR4 gene transcription. Enhanced CCR4 expression is associated with enhanced migration and proliferation. Furthermore, HBZ induced expression of TIGIT, which suppressed host immune response through increased IL-10 production from dendritic cells and T cells. HBZ causes inflammation through increased interferon gamma production.

Free Research Field

血液内科学