人类T细胞白血病病毒1型 (HTLV-1)是引起成人T细胞白血病（ATL）或淋巴瘤的病原体。我们的前期研究发现HTLV-1 Tax蛋白在促进Bcl3高表达的同时NFκB通路也被活化，而转入Bcl3表达载体使细胞中Bcl3过表达的时候，NFκB通路的活性却被抑制，并且Bcl3能够促进病毒感染细胞自噬，但这些结果的详细机制并不清楚。我们拟利用透射电子显微镜、共聚焦显微镜等仪器，采用免疫荧光染色、基因表达质粒转染、荧光素酶报告基因、TALENs和Westernblot 等方法，从分子和细胞水平探讨游离的Bcl3和与Tax蛋白结合的Bcl3对NFκB通路的作用机制，以及Bcl3促进细胞自噬的分子机制，从而确定Bcl3在HTLV-1病毒引起ATL中的关键作用，为将Bcl3作为阻止HTLV-1 病毒复制和ATL 发生的重要基因靶点，建立起有效的基因治疗方法奠定基础。

Human T-cell leukemia virus type 1 (HTLV - 1) is the pathogen caused adult T cell leukemia (ATL) / lymphoma. Recently, we found that HTLV-1 Tax protein could facilitate the Bcl3 expression and the activity of NFκB pathway, but the activity of NFκB pathway was inhibited when the Bcl3 gene over expression after the plasmids of Bcl3 expression were transfected into cells, and Bcl3 could promote the autophagy in HTLV-1 infected cells, but the mechanism is not clear. We will investigate the acting mechanism of free Bcl3 and Bcl3-Tax complex on NFκB pathway, and the molecular mechanism of Bcl3 promoting autophagy from molecular and cellular levels by the methods of immune fluorescence staining, transfection of gene expression plamids,luciferase reporter gene, TALENs technology and western blot etc., and using the instrument of transmission electron microscope, confocal microscope etc.It will be determined that Bcl3 play a key role in the pathogenesis of ATL caused by HTLV-1 virus, the results will lay the foundation of Bcl3 as the target of gene therapy to inhibit HTLV-1 viral replication and ATL occurrence.