Mononuclear Cells From Human Neonates Are Partially Resistant to the Action of 1, 25-Dihydroxyvitamin D

1, 25-Dihydroxyvitamin D [1, 25-(OH)₂D] inhibits mitogen-induced proliferation of lymphocytes by a receptormediated mechanism. Peripheral blood lymphocytes may serve as a model for detecting hereditary defects in the response of classical target organs to 1, 25-(OH)₂D. Delayed bone mineralization and deficient intestinal calcium absorption are common in low birth weight formula-fed infants. The defect in calcium absorption exists despite normal or even elevated serum 1, 25-(OH)₂D levels, suggesting partial end-organ resistance to the hormone. We assessed the response to 1, 25-(OH)₂D of activated mononuclear cells obtained from cord blood of fullterm and preterm infants and from peripheral blood of adults. We found that the inhibitory effect of 1, 25-(OH)₂D on mitogen-induced [³H]thymidine incorporation was significantly less [mean, 34 ± 8% (±se)] in mononuclear cells from neonates (independent of gestational age) compared to mononuclear cells from adults (66 ± 5%; P < 0.001). This difference in the inhibitory effect was not due to a smaller number of high affinity receptors for 1, 25-(OH)₂D in activated cord blood lymphocytes. We conclude that the coupling between the receptors for 1, 25-(OH)₂D and the biological response in neonates is less efficient than that in adults.