NOD1 modulates IL-10 signalling in human dendritic cells

Abstract NOD1 belongs to the family of NOD-like receptors, which is a group of well-characterised, cytosolic pattern-recognition receptors. The best-studied function of NOD-like receptors is their role in generating immediate pro-inflammatory and antimicrobial responses by detecting specific bacteri...

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Autores principales: Theresa Neuper, Kornelia Ellwanger, Harald Schwarz, Thomas A. Kufer, Albert Duschl, Jutta Horejs-Hoeck
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Lenguaje:EN
Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/b56c9e513c3647978deadd3230b4f077
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spelling oai:doaj.org-article:b56c9e513c3647978deadd3230b4f0772021-12-02T16:07:00ZNOD1 modulates IL-10 signalling in human dendritic cells10.1038/s41598-017-00691-x2045-2322https://doaj.org/article/b56c9e513c3647978deadd3230b4f0772017-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00691-xhttps://doaj.org/toc/2045-2322Abstract NOD1 belongs to the family of NOD-like receptors, which is a group of well-characterised, cytosolic pattern-recognition receptors. The best-studied function of NOD-like receptors is their role in generating immediate pro-inflammatory and antimicrobial responses by detecting specific bacterial peptidoglycans or by responding to cellular stress and danger-associated molecules. The present study describes a regulatory, peptidoglycan-independent function of NOD1 in anti-inflammatory immune responses. We report that, in human dendritic cells, NOD1 balances IL-10-induced STAT1 and STAT3 activation by a SOCS2-dependent mechanism, thereby suppressing the tolerogenic dendritic cell phenotype. Based on these findings, we propose that NOD1 contributes to inflammation not only by promoting pro-inflammatory processes, but also by suppressing anti-inflammatory pathways.Theresa NeuperKornelia EllwangerHarald SchwarzThomas A. KuferAlbert DuschlJutta Horejs-HoeckNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Theresa Neuper
Kornelia Ellwanger
Harald Schwarz
Thomas A. Kufer
Albert Duschl
Jutta Horejs-Hoeck
NOD1 modulates IL-10 signalling in human dendritic cells
description Abstract NOD1 belongs to the family of NOD-like receptors, which is a group of well-characterised, cytosolic pattern-recognition receptors. The best-studied function of NOD-like receptors is their role in generating immediate pro-inflammatory and antimicrobial responses by detecting specific bacterial peptidoglycans or by responding to cellular stress and danger-associated molecules. The present study describes a regulatory, peptidoglycan-independent function of NOD1 in anti-inflammatory immune responses. We report that, in human dendritic cells, NOD1 balances IL-10-induced STAT1 and STAT3 activation by a SOCS2-dependent mechanism, thereby suppressing the tolerogenic dendritic cell phenotype. Based on these findings, we propose that NOD1 contributes to inflammation not only by promoting pro-inflammatory processes, but also by suppressing anti-inflammatory pathways.
format article
author Theresa Neuper
Kornelia Ellwanger
Harald Schwarz
Thomas A. Kufer
Albert Duschl
Jutta Horejs-Hoeck
author_facet Theresa Neuper
Kornelia Ellwanger
Harald Schwarz
Thomas A. Kufer
Albert Duschl
Jutta Horejs-Hoeck
author_sort Theresa Neuper
title NOD1 modulates IL-10 signalling in human dendritic cells
title_short NOD1 modulates IL-10 signalling in human dendritic cells
title_full NOD1 modulates IL-10 signalling in human dendritic cells
title_fullStr NOD1 modulates IL-10 signalling in human dendritic cells
title_full_unstemmed NOD1 modulates IL-10 signalling in human dendritic cells
title_sort nod1 modulates il-10 signalling in human dendritic cells
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/b56c9e513c3647978deadd3230b4f077
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AT korneliaellwanger nod1modulatesil10signallinginhumandendriticcells
AT haraldschwarz nod1modulatesil10signallinginhumandendriticcells
AT thomasakufer nod1modulatesil10signallinginhumandendriticcells
AT albertduschl nod1modulatesil10signallinginhumandendriticcells
AT juttahorejshoeck nod1modulatesil10signallinginhumandendriticcells
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