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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Nature Portfolio
2017
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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) |
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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 |
work_keys_str_mv |
AT theresaneuper nod1modulatesil10signallinginhumandendriticcells AT korneliaellwanger nod1modulatesil10signallinginhumandendriticcells AT haraldschwarz nod1modulatesil10signallinginhumandendriticcells AT thomasakufer nod1modulatesil10signallinginhumandendriticcells AT albertduschl nod1modulatesil10signallinginhumandendriticcells AT juttahorejshoeck nod1modulatesil10signallinginhumandendriticcells |
_version_ |
1718384800497139712 |