He Lab

My laboratory is interested in the mechanisms regulating T cell differentiation and functions. Our work focus on IL-17 producing CD4+ T lymphocytes (also known as TH17 cells) which mediate pathogenic immunity involved in autoimmune diseases, and participate in protective immunity against bacterial and fungal infections.

TH17 cells are selected by pharmaceutical industries as the target to develop therapeutic treatments for autoimmune diseases. However, TH17 cells polarized under canonical conditions (IL-6 and TGFβ) are not able to induce autoimmunity unless presence of IL-23, implicating unique pathogenic TH17 populations. For instance, TH17 cells are present in the normal intestine, and are crucial to maintain homeostasis, defense pathogen infections (defensive TH17), and as well Inflammatory Bowel Diseases (IBD) which fall into the class of autoimmune diseases (pathogenic TH17). How pathogenic TH17 cells are regulated and how to identify drugs specifically target TH17-mediated pathology while sparing its physical functions in gut is largely unknown. 

We are currently exploring the features of intestinal TH17 populations under various circumstances: homeostasis, pathogen infection (defensive TH17), autoimmune bowel diseases (pathogenic TH17), with the aim to determine molecular mechanisms specifically regulating the commitment of pathogenic TH17 in vivo and identify novel molecules as specific targets for treating IBD. 

Another part of our current research is to develop novel ex vivo and in vivo assays to assess the pathology of mutations identified from IBD patients’ genomes. These findings will lead to better understanding of genetic predisposition of autoimmune diseases and establishment of approaches screening for people genetically susceptive to IBD.