IL-21-mediated non-canonical pathway for IL-1β production in conventional dendritic cells

Chi-Keung Wan, Peng Li, Rosanne Spolski, Jangsuk Oh, Allison B. Andraski, Ning Du, Zu-Xi Yu, Christopher P. Dillon, Douglas R. Green and Warren J. Leonard ()
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Chi-Keung Wan: Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung and Blood Institute, National Institutes of Health
Peng Li: Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung and Blood Institute, National Institutes of Health
Rosanne Spolski: Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung and Blood Institute, National Institutes of Health
Jangsuk Oh: Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung and Blood Institute, National Institutes of Health
Allison B. Andraski: Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung and Blood Institute, National Institutes of Health
Ning Du: Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung and Blood Institute, National Institutes of Health
Zu-Xi Yu: Pathology Core, National Heart, Lung and Blood Institute, National Institutes of Health
Christopher P. Dillon: St Jude Children’s Research Hospital
Douglas R. Green: St Jude Children’s Research Hospital
Warren J. Leonard: Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung and Blood Institute, National Institutes of Health

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: Abstract The canonical pathway for IL-1β production requires TLR-mediated NF-κB-dependent Il1b gene induction, followed by caspase-containing inflammasome-mediated processing of pro-IL-1β. Here we show that IL-21 unexpectedly induces IL-1β production in conventional dendritic cells (cDCs) via a STAT3-dependent but NF-κB-independent pathway. IL-21 does not induce Il1b expression in CD4+ T cells, with differential histone marks present in these cells versus cDCs. IL-21-induced IL-1β processing in cDCs does not require caspase-1 or caspase-8 but depends on IL-21-mediated death and activation of serine protease(s). Moreover, STAT3-dependent IL-1β expression in cDCs at least partially explains the IL-21-mediated pathologic response occurring during infection with pneumonia virus of mice. These results demonstrate lineage-restricted IL-21-induced IL-1β via a non-canonical pathway and provide evidence for its importance in vivo.

Date: 2015
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DOI: 10.1038/ncomms8988

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