Education

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.

Professional Experience

2005-2009, Postdoctoral 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.

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 the regulation 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.

Selected Publications

1. 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.

2. 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.

3. 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.

4.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.

5. 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.Immunity.31: 72-83.

6.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.

7.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.