After severe injury the immune system loses its ability to defend the body against infection by bacteria and viruses, leading to a high rate of infectious complications and mortality among trauma patients. The immune system is comprised of two components, the adaptive and innate systems, which cooperate to protect the body from invasion of foreign organisms. In healthy individuals, adaptive immune cells (i.e., T cells) receive instruction from innate cells such as macrophages and dendritic cells (also called antigen presenting cells, or APCs). Severe injury disrupts the communication between the innate and adaptive immune systems, rendering individuals susceptible to infection. In addition to direct regulation by APCs, a population of innate lymphocytes called natural killer T (NKT) cells can also regulate T cell immunity. APCs express a molecule called CD1d, that exclusively stimulates NKT cells to turn on genes that can either amplify protective T cell immunity, or turn it off all together. Recent studies by Dr. Faunce ’s laboratory have identified a central regulatory role for CD1d-NKT cell interactions in the control of T cell immunity after injury. Additional lines of experimentation in the Faunce laboratory examine how age affects NK and NKT cell effector functions and how NKT cells regulate the inflammatory response associated with cutaneous wound healing. As an immunologist and member of the Burn and Shock Trauma Institute, Dr. Faunce's main research objectives are to 1) understand the contributions of APCs, CD1d, and NKT cells to injury-related immune suppression and wound healing, 2) to identify possible immune cell-based therapeutic approaches for alleviating the immune defects that follow severe trauma, and 3) to understand the basic biology of NKT cells with regard to regulation of peripheral immunity and inflammation.