Abstract
Newborn animals generally mount poor T cell-mediated immune responses in vivo. As a result, neonates fall prey to infectious agents and diseases which have little impact on immunocompetent adult animals. For some time, it was believed that this phenomenon was due to an intrinsic inability of newborns to mount developmentally mature Th1 responses. Recent studies in mice have challenged that view; under certain conditions, adult-level Th1 function has been achieved in newborns. More often, however, neonates develop Th2-dominant responses. A major challenge in the field of developmental immunology is to understand why the 'default' response for neonates is Th2 function. Cell intrinsic as well as environmental influences may contribute to Th2 skewing in neonates.