Lack of Cell Cycle Inhibitor p21 and Low CD4+ T Cell Suppression in Newborns After Exposure to IFN-β

Jop Jans*, Wendy W. Unger, Elisabeth A.M. Raeven, Elles R. Simonetti, Marc J. Eleveld, Ronald de Groot, Marien I. de Jonge, Gerben Ferwerda

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Type I IFNs, such as interferon alpha and interferon beta, are key regulators of the adaptive immune response during infectious diseases. Type I IFNs are induced upon infection, bind interferon α/β receptors on T-cells and activate intracellular pathways. The activating and inhibitory consequences of type I IFN-signaling are determined by cell type and cellular environment. The neonatal immune system is associated with increased vulnerability to infectious diseases which could partly be explained by an immature CD4+ T-cell compartment. Here, we show low IFN-β-mediated inhibition of CD4+ T-cell proliferation, phosphorylation of retinoblastoma protein and cytokine production in human newborns compared to adults. In addition, both naïve and total newborn CD4+ T-cells are unable to induce the cell-cycle inhibitor p21 upon exposure to IFN-β in contrast to adults. The distinct IFN-β-signaling in newborns provides novel insights into T cell functionality and regulation of T cell-dependent inflammation during early life immune responses.

Original languageEnglish
Article number652965
JournalFrontiers in Immunology
Publication statusPublished - 12 Apr 2021

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© Copyright © 2021 Jans, Unger, Raeven, Simonetti, Eleveld, de Groot, de Jonge and Ferwerda.


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