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SummaryLymphokine production by newborn lymphocytes was assessed by measuring migration inhibition factor (MIF) and leukocyte inhibition factor (LIF) of isolated mononuclear cells from cord blood, 1-7-days-old newborns, and adult controls. Ficoll-Hypaque separated mononuclear cells were stimulated with phytohemagglutinin (PHA) or allogeneic lymphocytes in a mixed leukocyte culture (MLC), and the supernatants were harvested at optimal times for lymphokine assays. Thymidine incorporation into DNA was also assayed to calculate a proliferative index. M I F was assessed by the inhibition of adult mononuclear phagocyte cell migration under agarose; LIF was assessed by polymorphonuclear cell migration under agarose. Although the proliferative responses of cord and newborn cells are equivalent or greater than those of adult controls, the PHA-induced MIF production in cord blood and newborn lymphocytes was only 46% and 12.5% respectively of mean adult levels; MLC-induced MIF production was 44% and 7%. resoectivelv of mean adult levels. PHA-induced LIF productheir studies of lymphotoxin production in cord blood. We recently reported deficient immune interferon production despite normal classical interferon production, suggesting selective lymphokine abnormalities among newborns (3). Utilizing many of the same supernatants generated during the interferon studies, we measured MIF and LIF activity in cord blood lymphocytes and newborn lymphocytes after activation with PHA or allogeneic lymphocytes in a MLC.A new adaptation of the agarose chemotactic assay (10) was used to measure MIF in the supernatant of cultured cells and the Clausen modification of the polymorphonuclear leukocyte migration under agarose assay was used to measure LIF. Timed samples were obtained to determine the kinetics of lymphokine production. We found that after serial dilutions of the supernatants there were significant differences in both MIF and LIF production among newborn, cord, and adult cells. MATERIALS AND METHODS .tion in cord blood was 27% of adult levels. These differences are only appreciated if dilutions of the supernatants are assayed. Simultaneous assay of MIF and LIF production in dilution of supernatants from adult lymphocytes showed higher LIF activity, whereas in cord lymphocytes MIF activity was greater than LIF activity. This further emphasizes the non-identity of MIF and LIF. These results indicate another abnormality of T cellular immunity in newborns not detected by T-cell enumeration or proliferative responses and parallels other defects in specialized T cell function such as cytotoxicity and immune interferon production. Despite normal thymic size and function, normal T cell numbers and subsets, and vigorous proliferative responses to mitogens, cellular immunity in the newborn human is functionally deficient. This is suggested by the newborns' enhanced susceptibility to viral infection (4, 17), diminished delayed cutaneous hypersensitivity reactions (2, 24), and selective abnormalities (when compared to adults) of in vitro mea...

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A new method, chemotaxis under agarose gel, was used to assess the directed motility of polymorphonuclear (PMN) and mononuclear (MN) phagocytes of 21 newborns, 71 infants and children, and 50 adults. This assay requires only small quantities of cells and is rapid, easy, reproducible, and provides a permanent record. The chemotactic substance was zymosan-activated human serum. Monocyte chemotaxis in the newborn was approximately 50% of adult control values, using the Boyden chamber (8.1 ± 2 cells per high-power field[HPF] [SE] in newborns compared to 17 ± 3 cells per HPF in adults), and 25% of adult control values, using the agarose method (50 ± 10 cells in newborns compared to 216 ± 15 cells in adults). Both are significant differences (P < .005). MN chemotaxis remains extremely low through age 5, and remains moderately reduced until age 10. PMN chemotaxis in the newborn was 82 ± 21 cells compared to adult controls of 300± 42 cells, also a significant difference (P < .05). PMN chemotaxis remains markedly depressed through age 2. Thereafter, PMN chemotaxis increases but remains significantly less than in adults until age 16. These chemotactic defects may play an important role in depressed delayed hypersensitivity skin tests, diminished inflammatory reactions, and increased susceptibility to infection present in the newborn and young infant.