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Research Article Free access | 10.1172/JCI117469

Interleukin 12 exerts a differential effect on the maturation of neonatal and adult human CD45R0- CD4 T cells.

U Shu, C E Demeure, D G Byun, F Podlaski, A S Stern, and G Delespesse

University of Montreal, Notre-Dame Hospital Research Center, Canada.

Find articles by Shu, U. in: PubMed | Google Scholar

University of Montreal, Notre-Dame Hospital Research Center, Canada.

Find articles by Demeure, C. in: PubMed | Google Scholar

University of Montreal, Notre-Dame Hospital Research Center, Canada.

Find articles by Byun, D. in: PubMed | Google Scholar

University of Montreal, Notre-Dame Hospital Research Center, Canada.

Find articles by Podlaski, F. in: PubMed | Google Scholar

University of Montreal, Notre-Dame Hospital Research Center, Canada.

Find articles by Stern, A. in: PubMed | Google Scholar

University of Montreal, Notre-Dame Hospital Research Center, Canada.

Find articles by Delespesse, G. in: PubMed | Google Scholar

Published October 1, 1994 - More info

Published in Volume 94, Issue 4 on October 1, 1994
J Clin Invest. 1994;94(4):1352–1358. https://doi.org/10.1172/JCI117469.
© 1994 The American Society for Clinical Investigation
Published October 1, 1994 - Version history
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Abstract

It is now recognized that IL-12 plays a predominant role in protective immunity against intracellular pathogens by promoting the development of T helper type 1 (Th1) responses. We here report the unexpected observations that IL-12 exerts differential effects on the maturation of "native" human CD4 T cells isolated from umbilical cord blood or from the blood of healthy adults. After priming in the presence of IL-12, naive cells of adult donors, defined as CD45R0- CD4+ T cells, acquire a Th1 phenotype whereas neonatal cells develop into effector cells producing high levels of IL-4 in addition to IFN-gamma. This effect of IL-12 on neonatal T cells is direct inasmuch as it is observed on highly purified CD4 T cells, however, it is not inhibited by CD8 T cells and natural killer cells. Unstimulated neonatal T cells which have been preincubated with IL-12 before the priming behave like adult T cells and acquire a Th1 phenotype after stimulation in the presence of IL-12. Given that IL-4 is a potent antagonist of Th1 responses, the finding that IL-12 promotes the maturation of neonatal T cells into IL-4 producers may explain the increased susceptibility of neonates to intracellular pathogens and should be taken into account for the development of vaccines to be used in the perinatal period.

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