Immune Signaling and Regulation (Hui XIAO)
Toll-like receptors (TLRs) superfamily comprises a large group of receptors, which have evolved to recognize a broad range of molecular signatures associated with microbes. By sensing the presence of invading pathogen or danger signals released by damaged tissue, TLRs activate highly conserved signaling network, whereby leads to the induction of a plethora of genes involved in inflammation, immune regulation or tissue remodeling. Despite TLRs play a pivotal role in host defense, inappropriate activation of TLR signaling has been associated with a variety of human diseases, including chronic inflammation and cancer. Nevertheless, the precise mechanisms underlying the role of TLRs in host defense and inflammation-associated diseases are largely unclear. The objectives of our research are aimed at uncovering the molecular mechanisms by which TLRs recognize pathogen, initiate inflammation and tailor adaptive immune response, thereby provide novel insights into development of new vaccines and treatment of virus-induced chronic inflammation and cancer. We will be primarily focusing on three lines of studies: 1) Decipher the signaling pathways by which TLRs regulate the expression of proinflammatory genes at post-transcriptional levels, providing new insights into constrain of inflammatory conditions. 2) Identify the mechanisms by which TLRs cross-talk with NLRs and RLRs in pathogen recognition as well as immune evasion mechanisms exerted by viruses, exploring novel vaccination strategies.3) Determine the molecular mechanisms by which inflammation promotes tumorigenesis, validating animal models for the screening and test of anti-cancer drugs.