Inflammatory bowel diseases (IBD) have been rising as an epidemic disease worldwide. IBD are chronic gastrointestinal disorders with a high mortality rate, especially in patients with ulcerative colitis (UC). Furthermore, recent studies indicate that gut imbalance and IBD are the risks of other autoimmune diseases. The hyperactive immune response is responsible for inflammation in colon and tissue-resident regulatory T cells (Tregs) are pivotal for immune suppression which maintains intestine homeostasis. We are interested in understanding how Tregs in colon become dysfunctional and how the imbalance circumstance subsequently leads to IBD by mouse models. Currently, we work on these parts:

1. The mechanism of an autoimmune disease-associated gene, Xiap, in colonic Treg under inflammatory stimulations.

2.  How XIAP is involved in the features and functions of colonic Treg subsets. 

3.  The role of XIAP in the interaction between gut immunity and microbiota.