Our research group is studying the molecular and cellular mechanism controlling human innate immunity and inflammation. Human innate immunity serves as a radar surveillance system capable of sensing danger and abnormal signals from the environment as well as signals within human bodies. Proper activation of innate immunity is essential for host defense against invading pathogens, wound healing following injury, as well as eradication of dead or malignant cancer cells. However, excessive or abnormal innate immunity and inflammation lead to serious inflammatory diseases such as cardiovascular diseases, diabetes, asthma, rheumatoid arthritis, as well as neurological inflammatory diseases. It is with no surprise that National Institute of Health has recently put together a major roadmap entitled "Inflammation is the common cause for human disease". Despite the significance of innate immunity and inflammation, the molecular and cellular mechanism underlying this process is not clearly understood. Many cell surface receptors and associated intracellular signaling molecules are critically involved in the proper regulation of human innate immunity network. Our group has unraveled function for several key intracellular proteins essential for mediating human innate immunity process. By employing techniques in experimental molecular biology, targeted disruption of selected genes in transgenic mice models, computational simulation of cellular signaling networks, and gathering genetic information from human patients, we are defining potential molecular targets for future intervention of chronic human inflammatory diseases.

In particular, we are examining molecular networks spanning from a key protein kinase called interlukin-1 receptor associated kinase 1 (IRAK-1). Our team has observed that IRAK-1 is functionally connected with the regulation of nuclear transcription factors as well as cytoplasmic signaling proteins. Genetic variations in IRAK-1 are associated with the risk of cardiovascular diseases, diabetes and aging. We are in the process of defining the functional domains within IRAK-1 molecule that are responsible for its diverse cellular function. Consequently, chemical strategies are being explored to selectively modulate its function and related inflammatory complications. Our research team is funded by research grants from the National Institute of Health.