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IL-23 and IL-2 activation of STAT5 is required for optimal IL-22 production in ILC3s during colitis
Drivers of IL-22 secretion by ILC3s Secretion of the cytokine interleukin-22 (IL-22) by innate lymphoid cells and intestinal T cells in the gut promotes epithelial integrity and provides protection against intestinal pathogens. Bauché et al. examined which cytokines and signal transducer and activator of transcription (STAT) proteins activate IL-22 production by group 3 innate lymphoid cells (ILC3s) in mice.
LAG3+ Regulatory T Cells Restrain Interleukin-23-Producing CX3CR1+ Gut-Resident Macrophages during Group 3 Innate Lymphoid Cell-Driven Colitis
Interleukin-22 (IL-22)-producing group 3 innate lymphoid cells (ILC3) maintains gut homeostasis but can also promote inflammatory bowel disease (IBD). The regulation of ILC3-dependent colitis remains to be elucidated. Here we show that Foxp3 + regulatory T cells (Treg cells) prevented ILC3-mediated colitis in an IL-10-independent manner. Treg cells inhibited IL-23 and IL-1β production from intestinal-resident CX3CR1 + macrophages but not CD103 + dendritic cells.
Webinar | Humanized mouse models in checkpoint inhibitor development
Humanized tumor xenograft mouse models are powerful experimental systems for studying in vivo interactions between human immune cells and human tumors. These models are generated by engrafting both human hematopoietic stem cells and human tumor tissue into immunodeficient mice, such as the NOD/SCID gamma (NSG) strain.
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