Cellular Immunity at Birth

Immunity in the infant has been extensively studied in the past and numerous investigations have been made into the development of specific immunity, the production of antibody and the passive transfer of antibody from the mother. On the other hand comparatively little work has been devoted to elucidating the complexities of the cellular response since Tunnicliff (1910) observed that phagocytosis by infants' leucocytes of streptococci, staphylococci and pneumococci was less active than in adults until the age of about 2 years. Subsequently it was demonstrated that the efficiency of phagocytosis was to a large extent determined by factors in the serum. In this connexion the studies of Mudd, Lucke, McCutcheon and Strumia (1929) were particularly important since they clarified our understanding of mechanisms by which serum enhances phagocytosis in the immunized animal and the role of antibody therein. Ward and Enders (1933) were able to elaborate upon these observations and correlated the effects of complement and antibody. They concluded that complement acts merely in the role of a catalyst which accelerates the effect of antibody. A similar view put forward by Topley and Wilson (1929) was that 'in normal serum the low concentration of specific antibodies necessitates the adjuvant action of a considerable amount of complement before its presence can be detected so that the complementary action appears to dominate the picture, while the high concentration of specific antibody in an immune serum reduces the complementary effect to a mere enhancement of an effect which takes place in its absence'. Ward and Enders (1933), in one of the few reports dealing with infants, found that the titre of complement in infants under the age of 1 year was as high as that in adults. It seemed probable, therefore, that the inferiority of phagocytosis in infancy might be due to substances other than complement. The findings of Gluck and Silverman (1957) are thus consistent with earlier work in that they showed that a phagocytosis-promoting factor was located in the a,, a2 and f-globulin fractions of the serum protein. Matoth (1952) produced evidence which suggested that infants' leucocytes were inherently less active than those of adults and considered that the effect of serum was unimportant in spite of the fact that he noted infant serum to be less potent than adult serum in promoting phagocytosis. The picture of cellular immunity in early infancy is thus incomplete and as much of the earlier work was carried out with immune sera and virulent micro-organisms their conclusions and results cannot be applied without due criticism to the explanation of the newborn infant's vulnerability to infections by bacteria of low pathogenicity. The present investigation was designed in the light of previous work to study the processes involved in normal phagocytosis by the leucocytes of cord blood and the functional interdependence of leucocyte and serum in the infant at birth.