Abstract
Previously demonstrated deficiencies of immune PHA-induced interferon (IF) by leucocytes of normal newborns could be the result of a functionally immature T cell, macrophage (macro) or both. We therefore studied PHA-induced (IF) production by macros and T cells from 23 cord and 13 adult bloods. After Fiooll-Hypaque (FH) separation of mononuclear (mono) cells, macros were separated by adherence and cultivated for 7 days. T cells (separated by E-Rosettes) were then added, macro-T cultures were stimulated with PHA, and supernatants harvested at 48 hrs. IF was assessed by a microassay using Trisomy 21 cells and encephalomyocarditis virus challenge. PHA stimulated macro-T cultures of autologous and nonautologous cells (9 adults) showed enhanced IF production (GMT 121±1 SD) as compared to FH mono cells (GMT 42±1 SD). Combinations of adult and cord cells were PHA-stimulated. No IF was detected in supernates from PHA-stimulated FH cord cells alone or macro-T cord combined cultures. Similarly combined cord macro and adult T cells produced minimal IF (GMT 14±3 SD). Cord T cells with adult macros showed enhanced IF production (GMT 195±2 SD). These results indicate that the cord macrophage is primarily responsible for the poor IF PHA induced response since the newborn T cell functions normally in the presence of adult macros. Thus a combination of impaired macro IF production and increased susceptibility of neonatal macro to viral replication may explain the enhanced severity of neonatal viral infections.
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