401. NOD1 modulates IL-10 signalling in human dendritic cells.
- Author
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Neuper T, Ellwanger K, Schwarz H, Kufer TA, Duschl A, and Horejs-Hoeck J
- Subjects
- Animals, Cells, Cultured, Dendritic Cells immunology, Dendritic Cells metabolism, Gene Silencing, HEK293 Cells, Humans, Phenotype, STAT1 Transcription Factor metabolism, STAT3 Transcription Factor metabolism, Signal Transduction, Suppressor of Cytokine Signaling Proteins metabolism, Dendritic Cells cytology, Interleukin-10 metabolism, Nod1 Signaling Adaptor Protein genetics, Nod1 Signaling Adaptor Protein metabolism, Peptidoglycan immunology
- 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.
- Published
- 2017
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