Nod/Ripk2 signaling in dendritic cells activates IL-17A–secreting innate lymphoid cells and drives colitis inT-bet−/−.Rag2−/−(TRUC) mice
Copyright policy )Nod/Ripk2 signaling in dendritic cells activates IL-17A–secreting innate lymphoid cells and drives colitis inT-bet−/−.Rag2−/−(TRUC) mice
SignificanceDisease mechanisms in inflammatory bowel disease (IBD) are incompletely understood. In this study, we analyzed the role of IL-17A–secreting innate lymphoid cells (ILCs) in a mouse model of microbiota-driven innate immune-mediated colitis. We report that the pathogenic IL-17A response in ILCs is controlled indirectly by microbial stimulation of dendritic cells (DCs) via the nucleotide-binding oligomerization domain containing (Nod)/receptor-interacting serine-threonine kinase 2 (Ripk2) signaling pathway and requires the cytokines IL-23 and IL-1. Insight into the complex interactions between various immune cells as demonstrated here for DCs and ILCs is a prerequisite for the development of more efficacious therapies in IBD.
- Cornell University United States
- Merck & Co. United States
- Brigham and Women's Faulkner Hospital United States
- Harvard University United States
Mice, Knockout, Bacteria, Interleukin-17, Bone Marrow Cells, Dendritic Cells, Interleukin-23, DNA-Binding Proteins, Intestines, Mice, Receptor-Interacting Protein Serine-Threonine Kinase 2, Receptor-Interacting Protein Serine-Threonine Kinases, Animals, Humans, Colitis, Ulcerative, T-bet Transcription Factor, Chemokines, T-Box Domain Proteins, Signal Transduction
Mice, Knockout, Bacteria, Interleukin-17, Bone Marrow Cells, Dendritic Cells, Interleukin-23, DNA-Binding Proteins, Intestines, Mice, Receptor-Interacting Protein Serine-Threonine Kinase 2, Receptor-Interacting Protein Serine-Threonine Kinases, Animals, Humans, Colitis, Ulcerative, T-bet Transcription Factor, Chemokines, T-Box Domain Proteins, Signal Transduction
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