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 receptor-mediated 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 less than 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.