Analysis of the Immunological Dysregulation Underlying Defective Interferon γ Secretion in the Human Neonate

Abstract

Host responses to a range of microorganisms, including bacteria, mycobacteria, yeasts, parasites, and viruses, are mediocre in the human neonate. In the case of severe bacterial infections, lack of preexisting antibody (Baker and Kasper 1976), decreased complement levels (Fischer and Pearlman 1961), or deficient functions of phagocytes (Weston et al. 1977) may be responsible for the inadequate handling of the microorganism. In the case of infection with intracellular microorganisms (and particularly viruses), antibody and phagocytosis are unlikely to play a decisive role in host defense, so that a T-cell-mediated defect has to be postulated in order to explain the unusual susceptibility of neonates to such infections (Bellanti and Hurtado 1976). The so-called immaturity of cell-mediated immunity in neonates has been difficult to substantiate. Indeed, the number of monocytes, B and T lymphocytes (Campbell et al. 1974), subpopulations of T cells (Hayward and Kurnick 1981), T lymphocyte proliferation induced by mitogens (Campbell et al. 1974), or allogeneic cells (Granberg et al. 1976) are known to be normal in neonates.