特聘教授 / 陽明臨床醫學研究所

EDUCATION AND POSITIONS HELD:

• M.D., National Yang-Ming University, 1984
• D.Phil., University of Oxford, UK, 1992
• Postdoctoral fellow, Stanford University, 1993
• Director, Institute of Clinical Medicine, Natl. Yang-Ming Univ., Taipei,Taiwan, 2010-present
• Distinguished Professor, Department of Microbiology and Immunology, Natl. Yang-Ming Univ., Taipei, Taiwan, 2007-present
• Professor, Department of Microbiology and Immunology, Natl. Yang-Ming Univ., Taipei, Taiwan ,2001-present
• Director, Immunology Research Center, Natl. Yang-Ming Univ., Taiwan, 2000-present
• Director, Immunology Research Center, Taipei Veterans’ General Hospital, Taiwan, 2005-present
• Co-appointed Senior Investigator, National Health Research Center, Taipei, Taiwan ,2004-present
• Co-appointed Senior Investigator, Academia Sinica, Taipei, Taiwan, 2004-present
• Distinguished Research Fellow, Academia Sinica, Taipei, Taiwan, 2009-present

HONORS:

• Oversea Ph.D., studentship, Minister of Education, 1988
• Robert Wood Johnson Fellowship, 1993
• Outstanding Researcher Award, National Science Council, 1999
• Outstanding Researcher Award, National Science Council, 2003
• The 8th TienTe Lee Biomedical Awards-Outstanding Awards, 2013

RESEARCH INTERESTS:

Immunobiology of antigen presenting cells: non-Toll-like Innate Immunity Receptors

DCs (dendritic cells) and macrophages (M师) can either activate host immunity via stimulating T cells, B cells, and NK cells, or downregulating immune system via inducing cell anergy or promoting the development of regulatory T cells (Treg). The recognition of self versus non-self antigen relies on the abundant innate receptors, such as TOLL-like receptors, TREM receptors and lectin receptors. We are especially interested in the functions of non-TLR innate receptors in viral infections, and the immunomodulatory effects of decoy receptor 3 (DcR3) to modulate the activities of M师 and DCs.
We have developed a platform technology to identify members of lectin and TREM receptors as the pattern recognition receptors to flaviviruses, influenza viruses, and K. pneumoniae. In vivo study demonstrates the potential to suppress tissue damage and hemorrhagic shock via Blocking pathogen-receptor interaction. This makes non-TLRs the ideal targets for anti-inflammatory therapy.

抗原呈現細胞之免疫生物學：非Toll-like先天免疫受體

樹突細胞及巨噬細胞可刺激T細胞，B細胞及NK細胞以活化宿主免疫系統；另一方面則可藉著引發細胞anergy或增進調控性(regulatory)T細 胞而減弱免疫反應。樹突細胞及巨噬細胞可經由細胞表面大量表現的innate receptors，如TOLL-like受體，TREM受體或凝集素(Lectin)受體來辨認自體和非自體抗原。我們實驗室的研究重點在於非 TOLL-like先天免疫受體在病毒感染時的功用及腫瘤壞死因子第三號誘餌受體在調控活化巨噬細胞及樹突細胞之免疫調節作用。
我們已發展出一平台技術用以篩選凝集素與TREM受體中可辨識黃熱病毒，流行性感冒病毒及克雷伯氏肺炎桿菌之受體。在生物體研究證實了可藉由阻斷致病原與 受體之交互作用而抑制組織受損及出血性休克之可能性，而這也使得非TOLL-like受體在抗發炎療法中為一理想之目標。