A defect in the antigen-presenting function of macrophages from neonatal mice

Abstract

The newborn mammal has a limited ability to mount an immune response^1–5. As the individual matures, the potential for immunological reactivity develops and expands. During the early period of relative immune incompetence, tolerance to some foreign antigens is easily induced^6,7. It is thought that the individual may be acquiring tolerance to self antigens during this period, hence its importance for immunological homeostasis. The contribution of mononuclear phagocytes to the initiation of immune responses is now well established. These phagocytes are essential for the development of various lymphocyte functions, in particular, those of the T lymphocytes. Most T-lymphocyte activities require that the macrophage take up and ‘present’ the antigen in a process modulated by the I region of the major histocompatibility gene complex (for review see ref. 8). Although some earlier studies^5,9–13 have indicated deficient macrophage function in the neonate, precise definition of the putative deficiency is lacking. We show here that macrophages from neonatal mice present antigen poorly and that this can be correlated with the small number of macrophages that bear Ia antigens.