厦门大学生命科学学院导师介绍：刘文贤

  刘文贤Wen-Hsien Liu Ph.D.
  教授，博士生导师
  免疫学(Immunology)
  课题组组长
  Tel: +86-592-2880332
  Email: whliu@xmu.edu.cn
  个人简历
  1996年，台湾大学获学士学位；
  1998年，台湾长庚大学获硕士学位；
  2005年，台湾阳明大学获博士学位 (与台湾中央研究院联合培养)；
  2005至2009年，台湾中央研究院分子生物研究所博士后；
  2009至2014年，美国Scripps研究所博士后；
  2015年至今，厦门大学生命科学学院教授；
  2016年，入选厦门市第二批台湾特聘专家；
  2017年，入选厦门市第九批双百计划。
  1996, B.Sc.Dept. of Botony, Taiwan University
  1998, M.Sc.Institute of Basic Medicine, Chang Gung University
  2005, Ph.D.Institute of Microbiology and Immunology, Yang Ming University
  2005-2009Postdoctoral Fellow, Institute of Molecular Biology, Academia Sinica
  2009-2014  Research Associate, The Scripps Research Institute, USA
  2015-Present, Professor, School of Life Sciences, Xiamen University
  研究领域（Research Area)
  Self-reactive T cells cause tissue damage and inflammation by compromising T cell tolerance, which employs three mechanisms: deletion, anergy and regulatory T cell-mediated suppression. Dysregulation of self-reactive T cells is a major driving force in many autoimmune diseases and inflammatory disorders. In addition, follicular helper T (TFH) cells, germinal center B (GC B) cells, and plasma cells play critical roles in humoral immune responses. Under disease conditions, these cells also contribute to the pathogenesis of autoimmunity and inflammatory diseases.Our laboratory will focus on studying theregulation of TFH, GC B, plasma cells, and T cell tolerance by post-transcriptional mechanisms, such as kinases, phosphatases, E3 ubiquitin ligases, and non-coding RNAs including microRNAs and long non-coding RNAs. The experimental approaches employed in our laboratory include gene expression profiling,in vitro and in vivo functional screening, generation and analysis of knockout/transgenic mice, and mouse models of human diseases. Our goals are: 1) to elucidate the molecular and cellular mechanisms underlying the generation and function of TFH, GC B, and plasma cells, as well as T cell tolerance, and 2) to establish the causative relationships between variouspost-transcriptional mechanisms and immune responses, autoimmunity and inflammatory diseases.
  自我反应T细胞通过破坏T细胞耐受造成组织损伤及炎症反应。T细胞耐受包含三种主要机制：清除、T细胞失能及调节T细胞介导的抑制作用。因此，自我反应T细胞的异常调节是引起众多自身免疫病和炎症病变的主要原因。TFH细胞，生发中心B细胞，和浆细胞分化的调节不仅影响正常体液免疫反应，同时也参与自身免疫和炎症疾病的產生。本课题组主要探讨基因的转录后的调节机制,例如Kinases、phosphatases、E3 ubiquitin ligases和包含microRNAs及long non-coding RNAs在内的non-coding RNAs对TFH细胞，生发中心B细胞，和浆细胞的分化以及T细胞耐受的调节。我们将利用基因表达谱分析，体内与体外功能筛选、基因敲除和转基因小鼠的构建与分析，以及自身免疫病和炎症疾病的小鼠模型的构建与分析,去探究上述参与转录后调节基因的功能。我们的目标是研究调节TFH细胞、生发中心B细胞，和浆细胞的分化与功能以及T细胞耐受的分子与细胞机制，并且阐明转录后调节与免疫应答、自身免疫病和炎症疾病之间的因果关系。
  代表性论文(Selected Publications, *co-first author, #corresponding author)
  1.W.-H. Liu*#,S. G. Kang*, Z. Huang*,C.-J. Wu,H.-Y. Jin,C. J. Maine,Y. Liu,J. Shepherd,M. Sabouri‐Ghomi,A. Gonzalez-Martin,S.Xu, A. Hoffmann, Y. Zheng,L.-F. Lu,N. Xiao, G. Fu#, C. Xiao#. (2016). A miR-155-Peli1-c-Rel pathway controls the generation and function of T follicular helper cells.J. Exp. Med. 213: 1901-1919.
  2. H.-W. Hsiao*, T.-S. Hsu*,W.-H. Liu, W.-C. Hsieh, T.-F. Chou, Y.-J. Wu, S.-T. Jiang and M.-Z. Lai. (2015). Deltex1 antagonizesHIF1-α and sustains the stability of regulatory T cellsin vivo.Nat. Commun.6: 6353.
  3. T.-H. Hsu, H.-W. Hsiao, P.-J. Wu,W.-H. Liu, and M.-Z. Lai. (2014). Deltex1 promotes Protein kinase C θ degradation and sustains Casitas b-lineage lymphoma expression.J. Immunol.193: 1672-1680.
  4. H. Y. Jin, H. Oda, M. Lai, R. L. Skalsky, K. Bethel, J. Shepherd, S. G. Kang,W.-H. Liu, M. Sabouri-Ghomi, B. R. Cullen, K. Rajewsky, and C. Xiao. (2013). MicroRNA-17~ 92 plays a causative role in lymphomagenesis by coordinating multiple oncogenic pathways.EMBO J.32: 2377-2391.
  5. S. G. Kang*, W.-H. Liu*, P. Lu*?, H. Y. Jin, H. W. Lim, J. Shepherd, D. Fremgen, E. Verdin, M. B. A. Oldstone, H. Qi, J. R. Teijaro and C. Xiao. (2013). MiR-17~92 family microRNAs are critical regulators of T follicular helper cell differentiation.Nat. Immunol. 14: 849-857.
  6. H.-W. Hsiao*,W.-H. Liu*,C.-J. Wang, Y.-H. Lo, Y.-H. Wu, S.-C. Jiang and M.-Z. Lai. (2009). Deltex1 is a novel NFAT target that promotes T cell anergy.Immunity31: 72-83.
  7. W.-H. Liu, H.-W. Hsiao, W.-I. Tsou, and M.-Z. Lai. (2007). Notch inhibits apoptosis by direct interference with XIAP ubiquitination and degradation. EMBO J. 26: 1660–1669.
  8.W.-H. Liu, and M.-Z. Lai. (2005). Deltex regulates T-cell activation by targeted degradation of active MEKK1.Mol. Cell Biol. 25: 1367–1378.