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

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 o...

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Vydáno v:Frontiers in immunology Ročník 12; s. 652965
Hlavní autoři: Jans, Jop, Unger, Wendy W., Raeven, Elisabeth A. M., Simonetti, Elles R., Eleveld, Marc J., de Groot, Ronald, de Jonge, Marien I., Ferwerda, Gerben
Médium: Journal Article
Jazyk:angličtina
Vydáno: Switzerland Frontiers Media S.A 12.04.2021
Témata:
CD4 T cells
immunity
Immunology
interferon beta
newborns
proliferation
respiratory syncytial virus
interferon beta
cyclic-dependent kinase inhibitor/p21
proliferation
cell cycle
CD4 T cells
newborns
immunity
respiratory syncytial virus
ISSN:1664-3224, 1664-3224
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Shrnutí: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.
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Edited by: Ilan Bank, Sheba Medical Center, Israel
Reviewed by: Ivan Maillard, University of Pennsylvania, United States; Andrew D. Wells, Children’s Hospital of Philadelphia, United States
This article was submitted to T Cell Biology, a section of the journal Frontiers in Immunology
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2021.652965