Wu Bin

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Wu Bin

Wu Bin
Nanyang Assistant Professor

Office: 03s-52
Telephone: +65 6592 7863
Email: wubin@ntu.edu.sg
Website: https://sites.google.com/site/wubinlab/

 

Education

  • B.Sc. in Biological Sciences, 2002.07-2006.06, School of Biological Sciences, Nanyang Technological University, Singapore
  • Ph.D. in Biochemistry, Biophysics and Structural Biology, 2006.07-2010.02, School of Biological Sciences, Nanyang Technological University, Singapore

Professional Experience

  • Nanyang Assistant Professor, School of Biological Sciences, NTU 2015.03-present
  • Charles A. King Research fellow Harvard Medical School & Boston Children’s Hospital 2013.10-2015.02
  • GSK-IDI Research fellow Harvard Medical School 2010.02-2013.09

Research Interest

Auto-immune Diseases, including a range of chronic conditions from mild Allergies and Arthritis (8-40% population), to more severe conditions like Crohn’s Disease and Systemic Lupus Erythomatosus (SLE, ~0.1% population), have become a increasing burden in developed countries, particularly in ageing societies. Despite the urgencies of the rising trend of Auto-immune Diseases, current treatments of such conditions are largely passive and only relieve the symptoms temporarily. Accumulating evidences suggested that an imbalanced innate immunity is the root of most of the symptoms. Understanding the regulatory mechanisms of the innate immunity will provide us with the right tools and knowledge to cure Auto-immune Diseases.

Only until recent years, new discoveries and characterizations of a variety of cellular receptors have filled in the gaps of our understanding about how innate immunity works. These receptors are present in a wide range of cell types in human body, not only in specialized immune cells, capable of sensing almost all pathogens and initiating the defense mechanism. There are several classes of pathogen recognition receptors (PRRs), including the well-known Toll-like receptors (TLRs), and more recently characterized RIG-I like RNA helicases (RLRs), C-type lectin receptors (CLRs), NOD-like receptors (NLRs), and AIM-2 like receptors (ALRs). These PRRs target specific types of pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). In many cases, PRRs have redundant and overlapping substrate specificities. Once activated, they will interact with their respective downstream signaling proteins called ‘adaptors’. Different pathways can often crosstalk with each other to initiate a robust and coordinated immune response. These sophisticated signal processing and amplification are usually carefully regulated at the adaptor level.

A weakened cellular innate immune system will compromise the host’s function in effectively detecting and clearing the pathogens and maintaining health. However, a hyperactive or an imbalanced innate immune system contributes to undesirable autoimmune diseases. For example, in the case of Crohn’s disease, accumulating evidence suggest that mutations in several PRRs (including RLRs and NLRP3) result in the clinical symptoms. In these cases, the equilibrium among the immune system, the symbiotic microbes and the environmental factors is disrupted. In addition, mutations in MDA5 (a member of RLR) will result in elevated Interferon levels in patients and cause Aicardi-Goutieres Syndrome (AGS) and SLE. However, the detailed mechanisms of how to balance signals from multiple PRRs remain largely unclear, particularly the mechanism of activation threshold of these pathways, and the potential crosstalk and feedback between different signaling pathways. My research will focus on understanding these specific innate immune signaling pathways, with an ultimate goal of curing autoimmune diseases, using a combination of biochemical, structural and cellular approaches.