The majority of early, in utero immune development occurs independent of antigen exposure. Only later during development can a fetus respond to antigens, and even then the response depends on the stage of fetal development and the nature of the antigen. At birth, the neonate is rapidly exposed to large numbers of potential pathogens. Although immunocompetent, the neonate is immunonaive and dependent on passively acquired maternal immunoglobulins, immune cells, and other substances from colostrum for protection. Neonates that suffer failure of passive transfer of maternal immunoglobulins may be at increased risk for disease; however, many other factors interact in conjunction with the level of passively acquired immunoglobulin to determine the occurrence of disease. These include, but are not limited to, management, environment, hygiene, infection pressure, virulence of organisms, and antibody specificity. In addition to immunoglobulins, colostrum contains large numbers of immune cells and cytokines. It is thought that the primary role for the cellular component of colostrum is to interact with the development of local immunity and to modulate active immunization of the neonatal intestine. In particular, T lymphocytes are thought to transfer immune functions and secrete cytokines. Although most of the major cytokines have been identified in colostrum and milk, their biologic effects on the neonate have yet to be determined.