For decades intestinal epithelial cells were thought of as passive barriers to luminal contents, cells involved in nutrient absorption and electrolyte secretion. Studies during the past 10 to 15 years have changed that concept as our understanding of mucosal immunity has evolved and as we have come to understand that the regulation of this system is unique in terms of cellular interactions and factors produced. The intestinal epithelial cell has moved to the forefront of these studies where it has been shown to be an active participant in mucosal immunoregulation and inflammation. Results of the earliest studies suggested that epithelial cells might be involved in immune regulation because they expressed a series of cell surface molecules that correlate with classical antigen presentation (class I and II MHC molecules). Later on, the expression of nonclassical class I molecules was identified on these cells as well, raising the possibility of novel forms of interactions with unique cell populations. This was followed by the observation that epithelial cells secrete cytokines and chemokines, which not only regulate mucosal immune responses but also regulate inflammatory responses. By such processes, the IEC has been proposed as being a bridge between innate and adaptive immunity. The recent description of Toll-like receptors on IECs adds further support to this concept. Clearly there is growing appreciation of the multifaceted role that the IEC plays in the gut. The work on IECs in the past year has helped to refine this role.